The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
Drugs used to cause dilation of the blood vessels.
Part of the arm in humans and primates extending from the ELBOW to the WRIST.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
The smallest divisions of the arteries located between the muscular arteries and the capillaries.
A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
The flow of BLOOD through or around an organ or region of the body.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
The continuation of the axillary artery; it branches into the radial and ulnar arteries.
The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.
A competitive inhibitor of nitric oxide synthetase.
The presence of an increased amount of blood in a body part or an organ leading to congestion or engorgement of blood vessels. Hyperemia can be due to increase of blood flow into the area (active or arterial), or due to obstruction of outflow of blood from the area (passive or venous).
A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
The circulation of blood through the CORONARY VESSELS of the HEART.
The veins and arteries of the HEART.
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
A value equal to the total volume flow divided by the cross-sectional area of the vascular bed.
A method of non-invasive, continuous measurement of MICROCIRCULATION. The technique is based on the values of the DOPPLER EFFECT of low-power laser light scattered randomly by static structures and moving tissue particulates.
A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.
The neural systems which act on VASCULAR SMOOTH MUSCLE to control blood vessel diameter. The major neural control is through the sympathetic nervous system.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
Paracrine substances produced by the VASCULAR ENDOTHELIUM with VASCULAR SMOOTH MUSCLE relaxation (VASODILATION) activities. Several factors have been identified, including NITRIC OXIDE and PROSTACYCLIN.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Arteries which arise from the abdominal aorta and distribute to most of the intestines.
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
An inhibitor of nitric oxide synthetase which has been shown to prevent glutamate toxicity. Nitroarginine has been experimentally tested for its ability to prevent ammonia toxicity and ammonia-induced alterations in brain energy and ammonia metabolites. (Neurochem Res 1995:200(4):451-6)
A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Drugs used to cause constriction of the blood vessels.
A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.
Recording of change in the size of a part as modified by the circulation in it.
The innermost layer of the three meninges covering the brain and spinal cord. It is the fine vascular membrane that lies under the ARACHNOID and the DURA MATER.
Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.
Regional infusion of drugs via an arterial catheter. Often a pump is used to impel the drug through the catheter. Used in therapy of cancer, upper gastrointestinal hemorrhage, infection, and peripheral vascular disease.
An essential amino acid that is physiologically active in the L-form.
Compounds or agents that combine with cyclooxygenase (PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES) and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of eicosanoids, prostaglandins, and thromboxanes.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
The circulation of the BLOOD through the LUNGS.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
An agent that blocks the release of adrenergic transmitters and may have other actions. It was formerly used as an antihypertensive agent, but is now proposed as an anti-arrhythmic.
A diverse group of agents, with unique chemical structures and biochemical requirements, which generate NITRIC OXIDE. These compounds have been used in the treatment of cardiovascular diseases and the management of acute myocardial infarction, acute and chronic congestive heart failure, and surgical control of blood pressure. (Adv Pharmacol 1995;34:361-81)
The nonstriated involuntary muscle tissue of blood vessels.
The vessels carrying blood away from the heart.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
A class of drugs that act by inhibition of potassium efflux through cell membranes. Blockade of potassium channels prolongs the duration of ACTION POTENTIALS. They are used as ANTI-ARRHYTHMIA AGENTS and VASODILATOR AGENTS.
An alkaloid found in opium but not closely related to the other opium alkaloids in its structure or pharmacological actions. It is a direct-acting smooth muscle relaxant used in the treatment of impotence and as a vasodilator, especially for cerebral vasodilation. The mechanism of its pharmacological actions is not clear, but it apparently can inhibit phosphodiesterases and it may have direct actions on calcium channels.
The process of exocrine secretion of the SWEAT GLANDS, including the aqueous sweat from the ECCRINE GLANDS and the complex viscous fluids of the APOCRINE GLANDS.
The arterial blood vessels supplying the CEREBRUM.
The TEMPERATURE at the outer surface of the body.
An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.
Relatively complete absence of oxygen in one or more tissues.
The recording of muscular movements. The apparatus is called a myograph, the record or tracing, a myogram. (From Stedman, 25th ed)
Cell membrane glycoproteins that are selectively permeable to potassium ions. At least eight major groups of K channels exist and they are made up of dozens of different subunits.
The circulation of the BLOOD through the vessels of the KIDNEY.
Calcitonin gene-related peptide. A 37-amino acid peptide derived from the calcitonin gene. It occurs as a result of alternative processing of mRNA from the calcitonin gene. The neuropeptide is widely distributed in neural tissue of the brain, gut, perivascular nerves, and other tissue. The peptide produces multiple biological effects and has both circulatory and neurotransmitter modes of action. In particular, it is a potent endogenous vasodilator.
The processes of heating and cooling that an organism uses to control its temperature.
A vasodilator used in the treatment of ANGINA PECTORIS. Its actions are similar to NITROGLYCERIN but with a slower onset of action.
The circulation of blood through the BLOOD VESSELS of the BRAIN.
A stable prostaglandin endoperoxide analog which serves as a thromboxane mimetic. Its actions include mimicking the hydro-osmotic effect of VASOPRESSIN and activation of TYPE C PHOSPHOLIPASES. (From J Pharmacol Exp Ther 1983;224(1): 108-117; Biochem J 1984;222(1):103-110)
A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.
Guanosine cyclic 3',5'-(hydrogen phosphate). A guanine nucleotide containing one phosphate group which is esterified to the sugar moiety in both the 3'- and 5'-positions. It is a cellular regulatory agent and has been described as a second messenger. Its levels increase in response to a variety of hormones, including acetylcholine, insulin, and oxytocin and it has been found to activate specific protein kinases. (From Merck Index, 11th ed)
A transient reddening of the face that may be due to fever, certain drugs, exertion, stress, or a disease process.
Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC
Compounds that bind to and block the stimulation of PURINERGIC P1 RECEPTORS.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
A white crystal or crystalline powder used in BUFFERS; FERTILIZERS; and EXPLOSIVES. It can be used to replenish ELECTROLYTES and restore WATER-ELECTROLYTE BALANCE in treating HYPOKALEMIA.
Central retinal artery and its branches. It arises from the ophthalmic artery, pierces the optic nerve and runs through its center, enters the eye through the porus opticus and branches to supply the retina.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Salts of nitrous acid or compounds containing the group NO2-. The inorganic nitrites of the type MNO2 (where M=metal) are all insoluble, except the alkali nitrites. The organic nitrites may be isomeric, but not identical with the corresponding nitro compounds. (Grant & Hackh's Chemical Dictionary, 5th ed)
A quaternary ammonium parasympathomimetic agent with the muscarinic actions of ACETYLCHOLINE. It is hydrolyzed by ACETYLCHOLINESTERASE at a considerably slower rate than ACETYLCHOLINE and is more resistant to hydrolysis by nonspecific CHOLINESTERASES so that its actions are more prolonged. It is used as a parasympathomimetic bronchoconstrictor agent and as a diagnostic aid for bronchial asthma. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1116)
The circulation of blood through the BLOOD VESSELS supplying the abdominal VISCERA.
Treatment process involving the injection of fluid into an organ or tissue.
A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)
The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)
A technique for measuring extracellular concentrations of substances in tissues, usually in vivo, by means of a small probe equipped with a semipermeable membrane. Substances may also be introduced into the extracellular space through the membrane.
The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.
A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.
The functions of the skin in the human and animal body. It includes the pigmentation of the skin.
Abnormally low BLOOD PRESSURE that can result in inadequate blood flow to the brain and other vital organs. Common symptom is DIZZINESS but greater negative impacts on the body occur when there is prolonged depravation of oxygen and nutrients.
A clinical manifestation of abnormal increase in the amount of carbon dioxide in arterial blood.
Therapeutic introduction of ions of soluble salts into tissues by means of electric current. In medical literature it is commonly used to indicate the process of increasing the penetration of drugs into surface tissues by the application of electric current. It has nothing to do with ION EXCHANGE; AIR IONIZATION nor PHONOPHORESIS, none of which requires current.
Arteries which supply the dura mater.
The state of activity or tension of a muscle beyond that related to its physical properties, that is, its active resistance to stretch. In skeletal muscle, tonus is dependent upon efferent innervation. (Stedman, 25th ed)
The part of the face that is below the eye and to the side of the nose and mouth.
Nitrous acid sodium salt. Used in many industrial processes, in meat curing, coloring, and preserving, and as a reagent in ANALYTICAL CHEMISTRY TECHNIQUES. It is used therapeutically as an antidote in cyanide poisoning. The compound is toxic and mutagenic and will react in vivo with secondary or tertiary amines thereby producing highly carcinogenic nitrosamines.
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord.
The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system.
Highly reactive compounds produced when oxygen is reduced by a single electron. In biological systems, they may be generated during the normal catalytic function of a number of enzymes and during the oxidation of hemoglobin to METHEMOGLOBIN. In living organisms, SUPEROXIDE DISMUTASE protects the cell from the deleterious effects of superoxides.
Elements of limited time intervals, contributing to particular results or situations.
An element with atomic symbol O, atomic number 8, and atomic weight [15.99903; 15.99977]. It is the most abundant element on earth and essential for respiration.
A class of cell surface receptors that prefer ADENOSINE to other endogenous PURINES. Purinergic P1 receptors are widespread in the body including the cardiovascular, respiratory, immune, and nervous systems. There are at least two pharmacologically distinguishable types (A1 and A2, or Ri and Ra).
A cyclic nucleotide phosphodiesterase subfamily that is highly specific for CYCLIC GMP. It is found predominantly in vascular tissue and plays an important role in regulating VASCULAR SMOOTH MUSCLE contraction.
Delivery of drugs into an artery.
A group of organic sulfur-containing nitrites, alkyl thionitrites. S-Nitrosothiols include compounds such as S-NITROSO-N-ACETYLPENICILLAMINE and S-NITROSOGLUTATHIONE.
A prostaglandin that is a powerful vasodilator and inhibits platelet aggregation. It is biosynthesized enzymatically from PROSTAGLANDIN ENDOPEROXIDES in human vascular tissue. The sodium salt has been also used to treat primary pulmonary hypertension (HYPERTENSION, PULMONARY).
An alpha-1 adrenergic agonist that causes prolonged peripheral VASOCONSTRICTION.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
Adrenergic beta-2 agonist used as bronchodilator for emphysema, bronchitis and asthma.
Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)
Potassium channels whose activation is dependent on intracellular calcium concentrations.
Expenditure of energy during PHYSICAL ACTIVITY. Intensity of exertion may be measured by rate of OXYGEN CONSUMPTION; HEAT produced, or HEART RATE. Perceived exertion, a psychological measure of exertion, is included.
A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant.
The main trunk of the systemic arteries.
Abnormal enlargement or swelling of a KIDNEY due to dilation of the KIDNEY CALICES and the KIDNEY PELVIS. It is often associated with obstruction of the URETER or chronic kidney diseases that prevents normal drainage of urine into the URINARY BLADDER.
The measure of the level of heat of a human or animal.
A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.
A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters.
A 20-carbon-chain fatty acid, unsaturated at positions 8, 11, and 14. It differs from arachidonic acid, 5,8,11,14-eicosatetraenoic acid, only at position 5.
The main artery of the thigh, a continuation of the external iliac artery.
The movement of the BLOOD as it is pumped through the CARDIOVASCULAR SYSTEM.
A genus of the family Muridae having three species. The present domesticated strains were developed from individuals brought from Syria. They are widely used in biomedical research.
A subclass of adenosine A2 receptors found in LEUKOCYTES, the SPLEEN, the THYMUS and a variety of other tissues. It is generally considered to be a receptor for ADENOSINE that couples to the GS, STIMULATORY G-PROTEIN.
Studies comparing two or more treatments or interventions in which the subjects or patients, upon completion of the course of one treatment, are switched to another. In the case of two treatments, A and B, half the subjects are randomly allocated to receive these in the order A, B and half to receive them in the order B, A. A criticism of this design is that effects of the first treatment may carry over into the period when the second is given. (Last, A Dictionary of Epidemiology, 2d ed)
A phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells. Dipyridamole also potentiates the antiaggregating action of prostacyclin. (From AMA Drug Evaluations Annual, 1994, p752)
Cell surface proteins that bind ENDOTHELINS with high affinity and trigger intracellular changes which influence the behavior of cells.
The volume of BLOOD passing through the HEART per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with STROKE VOLUME (volume per beat).
A type of stress exerted uniformly in all directions. Its measure is the force exerted per unit area. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
Drugs that bind to but do not activate ADRENERGIC RECEPTORS. Adrenergic antagonists block the actions of the endogenous adrenergic transmitters EPINEPHRINE and NOREPINEPHRINE.
Any of the ruminant mammals with curved horns in the genus Ovis, family Bovidae. They possess lachrymal grooves and interdigital glands, which are absent in GOATS.
A group of conditions that develop due to overexposure or overexertion in excessive environmental heat.
A guanidine that opens POTASSIUM CHANNELS producing direct peripheral vasodilatation of the ARTERIOLES. It reduces BLOOD PRESSURE and peripheral resistance and produces fluid retention. (Martindale The Extra Pharmacopoeia, 31st ed)
21-Amino-acid peptides produced by vascular endothelial cells and functioning as potent vasoconstrictors. The endothelin family consists of three members, ENDOTHELIN-1; ENDOTHELIN-2; and ENDOTHELIN-3. All three peptides contain 21 amino acids, but vary in amino acid composition. The three peptides produce vasoconstrictor and pressor responses in various parts of the body. However, the quantitative profiles of the pharmacological activities are considerably different among the three isopeptides.
A 37-amino acid residue peptide isolated from the scorpion Leiurus quinquestriatus hebraeus. It is a neurotoxin that inhibits calcium activated potassium channels.
A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of RAYNAUD DISEASE and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease.
Nerve cells where transmission is mediated by NITRIC OXIDE.
A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed)
The artery formed by the union of the right and left vertebral arteries; it runs from the lower to the upper border of the pons, where it bifurcates into the two posterior cerebral arteries.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.
A potassium-selective ion channel blocker. (From J Gen Phys 1994;104(1):173-90)
A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
A stable, non-explosive inhalation anesthetic, relatively free from significant side effects.
Compounds which inhibit or antagonize the biosynthesis or actions of phosphodiesterases.
Cell surface receptors that bind BRADYKININ and related KININS with high affinity and trigger intracellular changes which influence the behavior of cells. The identified receptor types (B-1 and B-2, or BK-1 and BK-2) recognize endogenous KALLIDIN; t-kinins; and certain bradykinin fragments as well as bradykinin itself.
Microscopy in which television cameras are used to brighten magnified images that are otherwise too dark to be seen with the naked eye. It is used frequently in TELEPATHOLOGY.
A colorimetric reagent for iron, manganese, titanium, molybdenum, and complexes of zirconium. (From Merck Index, 11th ed)
An alkaloid, originally from Atropa belladonna, but found in other plants, mainly SOLANACEAE. Hyoscyamine is the 3(S)-endo isomer of atropine.
Physical activity which is usually regular and done with the intention of improving or maintaining PHYSICAL FITNESS or HEALTH. Contrast with PHYSICAL EXERTION which is concerned largely with the physiologic and metabolic response to energy expenditure.
Left bronchial arteries arise from the thoracic aorta, the right from the first aortic intercostal or the upper left bronchial artery; they supply the bronchi and the lower trachea.
A potassium-channel opening vasodilator that has been investigated in the management of hypertension. It has also been tried in patients with asthma. (Martindale, The Extra Pharmacopoeia, 30th ed, p352)
Inorganic or organic salts and esters of nitric acid. These compounds contain the NO3- radical.
A methyl xanthine derivative from tea with diuretic, smooth muscle relaxant, bronchial dilation, cardiac and central nervous system stimulant activities. Theophylline inhibits the 3',5'-CYCLIC NUCLEOTIDE PHOSPHODIESTERASE that degrades CYCLIC AMP thus potentiates the actions of agents that act through ADENYLYL CYCLASES and cyclic AMP.
The application of heat to raise the temperature of the environment, ambient or local, or the systems for accomplishing this effect. It is distinguished from HEAT, the physical property and principle of physics.
Substances that influence the course of a chemical reaction by ready combination with free radicals. Among other effects, this combining activity protects pancreatic islets against damage by cytokines and prevents myocardial and pulmonary perfusion injuries.
An alkylamide found in CAPSICUM that acts at TRPV CATION CHANNELS.
A sulfur-containing alkyl thionitrite that is one of the NITRIC OXIDE DONORS.
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.
A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis.
Enzyme complexes that catalyze the formation of PROSTAGLANDINS from the appropriate unsaturated FATTY ACIDS, molecular OXYGEN, and a reduced acceptor.
Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the actions of endogenous or exogenous adrenergic agonists. Adrenergic alpha-antagonists are used in the treatment of hypertension, vasospasm, peripheral vascular disease, shock, and pheochromocytoma.
Heterocyclic compounds in which an oxygen is attached to a cyclic nitrogen.
Diet modification and physical exercise to improve the ability of animals to perform physical activities.
Use of electric potential or currents to elicit biological responses.
A syndrome of persistent PULMONARY HYPERTENSION in the newborn infant (INFANT, NEWBORN) without demonstrable HEART DISEASES. This neonatal condition can be caused by severe pulmonary vasoconstriction (reactive type), hypertrophy of pulmonary arterial muscle (hypertrophic type), or abnormally developed pulmonary arterioles (hypoplastic type). The newborn patient exhibits CYANOSIS and ACIDOSIS due to the persistence of fetal circulatory pattern of right-to-left shunting of blood through a patent ductus arteriosus (DUCTUS ARTERIOSUS, PATENT) and at times a patent foramen ovale (FORAMEN OVALE, PATENT).
A CALCIUM-independent subtype of nitric oxide synthase that may play a role in immune function. It is an inducible enzyme whose expression is transcriptionally regulated by a variety of CYTOKINES.
A group of compounds that are derivatives of beta- aminoethylbenzene which is structurally and pharmacologically related to amphetamine. (From Merck Index, 11th ed)
The inferior part of the lower extremity between the KNEE and the ANKLE.
Volume of circulating BLOOD. It is the sum of the PLASMA VOLUME and ERYTHROCYTE VOLUME.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A subtype of endothelin receptor found predominantly in the VASCULAR SMOOTH MUSCLE. It has a high affinity for ENDOTHELIN-1 and ENDOTHELIN-2.
A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include ADENINE and GUANINE, constituents of nucleic acids, as well as many alkaloids such as CAFFEINE and THEOPHYLLINE. Uric acid is the metabolic end product of purine metabolism.
A water-soluble polypeptide (molecular weight approximately 8,000) extractable from the corpus luteum of pregnancy. It produces relaxation of the pubic symphysis and dilation of the uterine cervix in certain animal species. Its role in the human pregnant female is uncertain. (Dorland, 28th ed)
A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).
Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.
The finer blood vessels of the vasculature that are generally less than 100 microns in internal diameter.
A histamine H1 antagonist with low sedative action but frequent gastrointestinal irritation. It is used to treat ASTHMA; HAY FEVER; URTICARIA; and RHINITIS; and also in veterinary applications. Tripelennamine is administered by various routes, including topically.
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.
A drug combination that contains THEOPHYLLINE and ethylenediamine. It is more soluble in water than theophylline but has similar pharmacologic actions. It's most common use is in bronchial asthma, but it has been investigated for several other applications.
A calcium channel blocker that is a class IV anti-arrhythmia agent.
Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic beta-antagonists are used for treatment of hypertension, cardiac arrhythmias, angina pectoris, glaucoma, migraine headaches, and anxiety.
The direct continuation of the brachial trunk, originating at the bifurcation of the brachial artery opposite the neck of the radius. Its branches may be divided into three groups corresponding to the three regions in which the vessel is situated, the forearm, wrist, and hand.
The active metabolite of ENALAPRIL and a potent intravenously administered angiotensin-converting enzyme inhibitor. It is an effective agent for the treatment of essential hypertension and has beneficial hemodynamic effects in heart failure. The drug produces renal vasodilation with an increase in sodium excretion.
A constitutively expressed subtype of bradykinin receptor that may play a role in the acute phase of the inflammatory and pain response. It has high specificity for intact forms of BRADYKININ and KALLIDIN. The receptor is coupled to G-PROTEIN, GQ-G11 ALPHA FAMILY and G-PROTEIN, GI-GO ALPHA FAMILY signaling proteins.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
The oxygen-carrying proteins of ERYTHROCYTES. They are found in all vertebrates and some invertebrates. The number of globin subunits in the hemoglobin quaternary structure differs between species. Structures range from monomeric to a variety of multimeric arrangements.
A nonsteroidal anti-inflammatory agent with analgesic properties used in the therapy of rheumatism and arthritis.
Ultrasonography applying the Doppler effect, with frequency-shifted ultrasound reflections produced by moving targets (usually red blood cells) in the bloodstream along the ultrasound axis in direct proportion to the velocity of movement of the targets, to determine both direction and velocity of blood flow. (Stedman, 25th ed)
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
The hollow, muscular organ that maintains the circulation of the blood.
Inorganic oxides that contain nitrogen.

Phospholamban is present in endothelial cells and modulates endothelium-dependent relaxation. Evidence from phospholamban gene-ablated mice. (1/8444)

Vascular endothelial cells regulate vascular smooth muscle tone through Ca2+-dependent production and release of vasoactive molecules. Phospholamban (PLB) is a 24- to 27-kDa phosphoprotein that modulates activity of the sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA). Expression of PLB is reportedly limited to cardiac, slow-twitch skeletal and smooth muscle in which PLB is an important regulator of [Ca2+]i and contractility in these muscles. In the present study, we report the existence of PLB in the vascular endothelium, a nonmuscle tissue, and provide functional data on PLB regulation of vascular contractility through its actions in the endothelium. Endothelium-dependent relaxation to acetylcholine was attenuated in aorta of PLB-deficient (PLB-KO) mice compared with wild-type (WT) controls. This effect was not due to actions of nitric oxide on the smooth muscle, because sodium nitroprusside-mediated relaxation in either denuded or endothelium-intact aortas was unaffected by PLB ablation. Relative to denuded vessels, relaxation to forskolin was enhanced in WT endothelium-intact aortas. The endothelium-dependent component of this relaxation was attenuated in PLB-KO aortas. To investigate whether these changes were due to PLB, WT mouse aorta endothelial cells were isolated. Both reverse transcriptase-polymerase chain reaction and Western blot analyses revealed the presence of PLB in endothelial cells, which were shown to be >98% pure by diI-acetylated LDL uptake and nuclear counterstaining. These data indicate that PLB is present and modulates vascular function as a result of its actions in endothelial cells. The presence of PLB in endothelial cells opens new fields for investigation of Ca2+ regulatory pathways in nonmuscle cells and for modulation of endothelial-vascular interactions.  (+info)

Loss of endothelium and receptor-mediated dilation in pial arterioles of rats fed a short-term high salt diet. (2/8444)

A high salt diet often is regarded as an accessory risk factor in hypertension, coincidental to the deleterious effect of high blood pressure on vasodilator function. The aim of this study was to determine whether short-term ingestion of a high salt diet per se impairs vasodilator function in the cerebral circulation independent of blood pressure changes. Adult Sprague-Dawley rats were fed a normal salt (0.8%) or high salt (4%) diet for 3 days. Mean arterial pressures were similar in the normal and high salt groups (123+/-2 and 125+/-2 mm Hg, respectively). Subsequently, the responses of the in situ pial arterioles to acetylcholine, iloprost, and sodium nitroprusside were determined in cranial windows using intravital videomicroscopy. Pial arterioles of rats fed normal and high salt diets showed similar resting diameters of 69+/-2 and 72+/-3 microm, respectively, but their reactivity patterns to vasodilator stimuli were markedly different. Arterioles of rats fed a normal salt diet dilated progressively up to 17+/-3% in response to the endothelium-dependent agent acetylcholine (10(-9) to 10(-6) mol/L) and dilated by 22+/-2% in response to the prostaglandin I2 receptor agonist iloprost (3x10(-11) mol/L). In contrast, pial arterioles of rats fed a high salt diet constricted by 4+/-3% and 8+/-2% in response to acetylcholine and iloprost, respectively. Sodium nitroprusside (10(-6) mol/L), a nitric oxide donor, dilated pial arterioles of rats fed low and high salt diets by a similar amount (19+/-3% and 16+/-2%, respectively), suggesting that signaling mechanisms for dilation distal to the vascular smooth muscle membrane were intact after high salt intake. These results provide the first evidence that the short-term ingestion of a high salt diet may severely impair the vasodilator function of the in situ cerebral microcirculation independent of blood pressure elevation.  (+info)

Role of nitric oxide-cGMP pathway in adrenomedullin-induced vasodilation in the rat. (3/8444)

We previously reported that adrenomedullin (AM), a potent vasodilator peptide discovered in pheochromocytoma cells, stimulates nitric oxide (NO) release in the rat kidney. To further investigate whether the NO-cGMP pathway is involved in the mechanisms of AM-induced vasodilation, we examined the effects of E-4021, a cGMP-specific phosphodiesterase inhibitor, on AM-induced vasorelaxation in aortic rings and perfused kidneys isolated from Wistar rats. We also measured NO release from the kidneys using a chemiluminescence assay. AM (10(-10) to 10(-7) mol/L) relaxed the aorta precontracted with phenylephrine in a dose-dependent manner. Denudation of endothelium (E) attenuated the vasodilatory action of AM (10(-7) mol/L AM: intact (E+) -25.7+/-5.2% versus denuded (E-) -7. 8+/-0.6%, P<0.05). On the other hand, pretreatment with 10(-8) mol/L E-4021 augmented AM-induced vasorelaxation in the intact aorta (-49. 0+/-7.9%, P<0.05) but not in the denuded one. E-4021 also enhanced acetylcholine (ACh)-induced vasorelaxation in the rat intact aorta (10(-7) mol/L ACh -36.6+/-8.4% versus 10(-8) mol/L E-4021+10(-7) mol/L ACh -62.7+/-3.1%, P<0.05). In perfused kidneys, AM-induced vasorelaxation was also augmented by preincubation with E-4021 (10(-9) mol/L AM -15.4+/-0.6% versus 10(-8) mol/L E-4021+10(-9) mol/L AM -23.6+/-1.2%, P<0.01). AM significantly increased NO release from rat kidneys (DeltaNO: +11.3+/-0.8 fmol. min-1. g-1 kidney at 10(-9) mol/L AM), which was not affected by E-4021. E-4021 enhanced ACh-induced vasorelaxation (10(-9) mol/L ACh -9.7+/-1.7% versus 10(-8) mol/L E-4021+10(-9) mol/L ACh -18.8+/-2.9%, P<0.01) but did not affect ACh-induced NO release from the kidneys. In the aorta and the kidney, 10(-4) mol/L of NG-nitro-L-arginine methyl ester, an NO synthase inhibitor, and 10(-5) mol/L of methylene blue, a guanylate cyclase inhibitor, reduced the vasodilatory effect of AM. These results suggest that the NO-cGMP pathway is involved in the mechanism of AM-induced vasorelaxation, at least in the rat aorta and kidney.  (+info)

Role of endothelin in the increased vascular tone of patients with essential hypertension. (4/8444)

We investigated the possible role of endothelin in the increased vasoconstrictor tone of hypertensive patients using antagonists of endothelin receptors. Forearm blood flow (FBF) responses (strain-gauge plethysmography) to intraarterial infusion of blockers of endothelin-A (ETA) (BQ-123) and endothelin-B (ETB) (BQ-788) receptors, separately and in combination, were measured in hypertensive patients and normotensive control subjects. In healthy subjects, BQ-123 alone or in combination with BQ-788 did not significantly modify FBF (P=0.78 and P=0.63, respectively). In hypertensive patients, in contrast, BQ-123 increased FBF by 33+/-7% (P<0.001 versus baseline), and the combination of BQ-123 and BQ-788 resulted in a greater vasodilator response (63+/-12%; P=0.006 versus BQ-123 alone in the same subjects). BQ-788 produced a divergent vasoactive effect in the two groups, with a decrease of FBF (17+/-5%; P=0.004 versus baseline) in control subjects and transient vasodilation (15+/-7% after 20 minutes) in hypertensive patients (P<0.001, hypertensives versus controls). The vasoconstrictor response to endothelin-1 was slightly higher (P=0.04) in hypertensive patients (46+/-4%) than in control subjects (32+/-4%). Our data indicate that patients with essential hypertension have increased vascular endothelin activity, which may be of pathophysiological relevance to their increased vascular tone. In these patients, nonselective ETA and ETB blockade seems to produce a greater vasodilator effect than selective ETA blockade.  (+info)

Microvascular function relates to insulin sensitivity and blood pressure in normal subjects. (5/8444)

BACKGROUND: A strong but presently unexplained inverse association between blood pressure and insulin sensitivity has been reported. Microvascular vasodilator capacity may be a common antecedent linking insulin sensitivity to blood pressure. To test this hypothesis, we studied 18 normotensive and glucose-tolerant subjects showing a wide range in insulin sensitivity as assessed with the hyperinsulinemic, euglycemic clamp technique. METHODS AND RESULTS: Blood pressure was measured by 24-hour ambulatory blood pressure monitoring. Videomicroscopy was used to measure skin capillary density and capillary recruitment after arterial occlusion. Skin blood flow responses after iontophoresis of acetylcholine and sodium nitroprusside were evaluated by laser Doppler flowmetry. Insulin sensitivity correlated with 24-hour systolic blood pressure (24-hour SBP; r=-0.50, P<0.05). Capillary recruitment and acetylcholine-mediated vasodilatation were strongly and positively related to insulin sensitivity (r=0.84, P<0.001; r=0.78, P<0.001, respectively), and capillary recruitment was inversely related to 24-hour SBP (r=-0.53, P<0.05). Waist-to-hip ratio showed strong associations with insulin sensitivity, blood pressure, and the measures of microvascular function but did not confound the associations between these variables. Subsequent regression analysis showed that the association between insulin sensitivity and blood pressure was not independent of the estimates of microvascular function, and part of the variation in both blood pressure (R2=38%) and insulin sensitivity (R2=71%) could be explained by microvascular function. CONCLUSIONS: Insulin sensitivity and blood pressure are associated well within the physiological range. Microvascular function strongly relates to both, consistent with a central role in linking these variables.  (+info)

Endothelial function in Marfan syndrome: selective impairment of flow-mediated vasodilation. (6/8444)

BACKGROUND: The cardiovascular complications of Marfan syndrome arise due to alterations in the structural and functional properties of fibrillin, a constituent of vascular connective tissues. Fibrillin-containing microfibrils are closely associated with arterial endothelial cells, indicating a possible functional role for fibrillin in the endothelium. Plasma concentrations of endothelial cell products are elevated in Marfan subjects, which indirectly indicates endothelial dysfunction. This study directly assessed flow- and agonist-mediated endothelium-dependent brachial artery reactivity in Marfan subjects. METHODS AND RESULTS: In 20 Marfan and 20 control subjects, brachial artery diameter, blood flow, and blood pressure were measured by ultrasonic wall tracking, Doppler ultrasound, and photoplethysmography, respectively. Measurements were taken during hand hyperemia (a stimulus for endothelium-derived nitric oxide [NO] release in the upstream brachial artery) and after sublingual administration of the endothelium-independent vasodilator nitroglycerin. In 9 Marfan and 6 control subjects, the above parameters were also assessed during intra-arterial infusions of acetylcholine and bradykinin (agonists that stimulate NO production) and NG-monomethyl-L-arginine (L-NMMA, an inhibitor of NO production). Flow-mediated responses differed markedly between Marfan and control subjects (-1.6+/-3.5% versus 6. 50+/-4.1%, respectively; P<0.0001), whereas nitroglycerin produced similar vasodilation (14.2+/-5.7% versus 15.2+/-7.8%; P=NS). Agonist-induced vasodilation to incremental intra-arterial infusions of acetylcholine and bradykinin were not significantly different between Marfan and control subjects, and intra-arterial L-NMMA produced similar reductions in brachial artery diameter in both groups. CONCLUSIONS: These data demonstrate impaired flow-mediated but preserved agonist-mediated endothelium-dependent vasodilation in Marfan subjects and suggest preservation of basal NO release. Selective loss of flow-mediated dilation suggests a role for fibrillin in endothelial cell mechanotransduction.  (+info)

Neurogenic vasodilatation of canine isolated small labial arteries. (7/8444)

Mechanisms underlying vasodilatation to nerve stimulation by electrical pulses and nicotine were analyzed in isolated canine small labial arteries. Transmural electrical stimulation (5 and 20 Hz) produced a contraction followed by a relaxation in labial arterial strips denuded of the endothelium, partially contracted with prostaglandin F2alpha. The contraction was abolished by prazosin or combined treatment with alpha, beta-methylene ATP. In the treated strips, neurogenic relaxation was abolished by NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthase inhibitor, and restored by L-arginine. The D-enantiomers were without effect. Nicotine (10(-4) M) also relaxed the arteries, in which the contractile response was abolished by prazosin and alpha, beta-methylene ATP. The relaxant response was attenuated but not abolished by L-NA; the inhibition was reversed by L-arginine. The remaining relaxation by nicotine was abolished by calcitonin gene-related peptide (CGRP)-[8 to 37], a CGRP1 receptor antagonist. Relaxations elicited by a lower concentration of nicotine (2 x 10(-5) M) sufficient to produce similar magnitudes of response to those induced by 5-Hz electrical nerve stimulation were also inhibited partially by L-NA. Histochemical study with the NADPH-diaphorase method demonstrated positively stained nerve fibers and bundles in the arterial wall, suggesting the presence of neuronal NO synthase. It is concluded that the relaxation induced by electrical nerve stimulation of small labial arteries is mediated exclusively by NO synthesized from L-arginine in nerve terminals, whereas nicotine in the concentrations used evokes relaxations by a mediation of nerve-derived NO and also CGRP, possibly from sensory nerves. The reason why nicotine but not electrical pulses stimulates sensory nerves and elicits vasorelaxation remains unsolved.  (+info)

Relaxation of endothelin-1-induced pulmonary arterial constriction by niflumic acid and NPPB: mechanism(s) independent of chloride channel block. (8/8444)

We investigated the effects of the Cl- channel blockers niflumic acid, 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) and 4, 4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) on endothelin-1 (ET-1)-induced constriction of rat small pulmonary arteries (diameter 100-400 microm) in vitro, following endothelium removal. ET-1 (30 nM) induced a sustained constriction of rat pulmonary arteries in physiological salt solution. Arteries preconstricted with ET-1 were relaxed by niflumic acid (IC50: 35.8 microM) and NPPB (IC50: 21.1 microM) in a reversible and concentration-dependent manner. However, at concentrations known to block Ca++-activated Cl- channels, DIDS (+info)

OBJECTIVES: A progressive decline in endothelium-dependent vasodilation (EDV) in the human forearm with age has previously been reported. The aim of this study was to evaluate the interplay between age, gender and metabolic factors on EDV in healthy subjects in a population-based study. SETTING: Tertiary university hospital. SUBJECTS AND DESIGN: Thirty-six healthy men and 30 women, aged 20-69 years, underwent measurements of forearm blood flow (FBF) at rest and during local infusions of 2 and 4 microg min-1 of metacholine (evaluating EDV) and 5 and 10 microg min-1 of sodium nitroprusside (evaluating endothelium-independent vasodilation, EIDV) and during reactive hyperaemia by venous occlusion plethysmography. RESULTS: Age was inversely related to EDV (r = - 0.41, P , 0.05 in men; r = - 0.61, P , 0.01 in women) and maximal FBF during reactive hyperaemia in both men and women. EIDV was significantly related to age in an inverse way in women only. EDV was more pronounced in females than in males ...
The present study demonstrates that long-term cigarette smoking is associated with impaired endothelium-dependent coronary vasodilation regardless of the presence or absence of atherosclerotic wall thickening. These findings extend previous observations obtained in the brachial artery to coronary arteries, suggesting that smoking is associated with a generalized endothelial vasodilator dysfunction. Most importantly, even in the presence of atherosclerotic wall thickening, smokers exhibited further impairment in flow-dependent coronary arterial dilation indicative of an additive adverse effect on endothelium-dependent coronary vasodilator function. Vasodilation in response to increased blood flow in conductance vessels was shown to be strictly dependent on an intact, normally functioning endothelium18 19 and is mediated by the signal of shear stress on the endothelial cell layer20 to release vasoactive factors like endothelium-derived relaxing factor (EDRF), believed to be nitric oxide or a ...
TY - JOUR. T1 - Changes in endothelium-dependent vasodilatation and alpha-adrenergic responses in resistance vessels during the menstrual cycle in healthy women. AU - Chan, N. Norman. AU - MacAllister, Raymond J.. AU - Colhoun, Helen M.. AU - Vallance, Patrick. AU - Hingorani, Aroon D.. N1 - 10.1210/jc.86.6.2499 Article 0021-972X. PY - 2001. Y1 - 2001. N2 - During the menstrual cycle, changes in endothelium-dependent vasodilatation have been demonstrated in conduit vessels in vivo, but responses in resistance vessels have not been studied. The aim of this study was to examine endothelium-dependent vasodilatation, the effects of local nitric oxide synthesis, and alpha-adrenergic constriction in resistance vessels during the menstrual cycle in 15 healthy female volunteers (mean age, 28.07 ± 2.1 yr). Forearm blood flow in response to intrabrachial infusion of bradykinin (10, 30, and 100 pmol/min; endothelium-dependent vasodilator), glyceryl trinitrate (4, 8, and 16 nmol/min; ...
TY - JOUR. T1 - Impaired endothelium-mediated vasodilation in the peripheral vasculature of patients with congestive heart failure. AU - Katz, Stuart D.. AU - Biasucci, Luigi. AU - Sabba, Carlo. AU - Strom, Joel A.. AU - Jondeau, Guillaume. AU - Galvao, Marie. AU - Solomon, Steven. AU - Nikolic, Srdjan D.. AU - Forman, Robert. AU - LeJemtel, Thierry H.. PY - 1992/4. Y1 - 1992/4. N2 - Impaired endothelial-dependent vasodilation has been demonstrated in two animal models of congestive heart failure and in the coronary circulation of patients with idiopathic dilated cardiomyopathy. To determine whether this impairment contributes to the abnormal peripheral vasomotor tone in patients with congestive heart failure, the local vascular response to intraarterial infusions of graded concentrations (10-8 M to 10-5 M) of acetylcholine (an endothelial-dependent vasodilator) and nitroglycerin (a direct-acting vasodilator) was studied in the superficial femoral artery of 19 patients with congestive heart ...
TY - JOUR. T1 - Endothelium removal augments endothelium-independent vasodilatation in rat mesenteric vascular bed. AU - Iwatani, Y.. AU - Kosugi, K.. AU - Isobe-Oku, S.. AU - Atagi, S.. AU - Kitamura, Yoshihisa. AU - Kawasaki, H.. PY - 2008/5. Y1 - 2008/5. N2 - Background and purpose: The vascular endothelium regulates vascular tone by releasing various endothelium-derived vasoactive substances to counteract excess vascular response. We investigated whether the vascular endothelium regulates vasodilatation via released endothelium-derived contracting factors (EDCFs), by examining the effect of endothelium removal on responses to periarterial nerve stimulation (PNS) and various vasodilator agents. Experimental approach: The rat mesenteric vascular bed was perfused with Krebs solution. Vasodilator responses to PNS and 5 min perfusion of vasodilator agents in preparations with endothelium were compared with those in the same preparations without endothelium. The endothelium was removed by 30 s ...
In acute ischaemia, glucose-insulin-potassium administration reduces mortality and β-adrenoceptor antagonists have favourable effects on the outcome of ischaemic heart disease. The present study was designed to investigate whether insulin (1.4×10−7 M) and the β-adrenoceptor antagonist, propranolol (10−5 M), increase hypoxic vasodilation in correspondence with changes in glycolysis. Porcine coronary arteries, precontracted with 10−5 M prostaglandin F2α, were mounted in a pressure myograph and a microdialysis catheter was inserted in the tunica media. Hypoxic vasodilation, interstitial lactate/pyruvate ratio and interstitial glucose were measured at low (2 mM) and high (20 mM) glucose concentrations. Hypoxia (60 min) caused vasodilation and doubled the lactate/pyruvate ratio. Treatment with insulin quadrupled the lactate/pyruvate ratio during hypoxia, but did not change hypoxic vasodilation. Propranolol blocked isoprenaline-evoked vasodilation, but hypoxic increases in lactate/pyruvate ...
ET (endothelin)-1, a potent vasoconstrictor peptide released by the endothelium, plays an important role in vasomotor regulation and has been linked to diminished endothelial vasodilator capacity in several pathologies associated with human aging, including hypertension, Type 2 diabetes and coronary artery disease. However, it is currently unknown whether the decline in endothelial vasodilatation with advancing age is due to elevated ET-1 vasconstrictor activity. Accordingly, we tested the hypothesis that the age-related impairment in ACh (acetylcholine)-mediated endothelium-dependent vasodilatation is due, at least in part, to increased ET-1-mediated vasoconstrictor tone. FBF (forearm blood flow) responses to ACh, SNP (sodium nitroprusside) and BQ-123 (ETA receptor blocker) were determined in 14 young (age, 25±1 years) and 14 older (age, 61±2 years) healthy non-obese men. Additionally, FBF responses to ACh were determined in the presence of ETA blockade. Vasodilatation to ACh was lower ...
Background: Several studies have shown that both early and late effects of ischemic preconditioning (IPC) protect against myocardial injury following ischemic reperfusion. Recently, we have shown that repetition of IPC stimulus augments endothelium-dependent vasodilation in forearm circulation of healthy subjects through increases in nitric oxide (NO) production and number of endothelial progenitor cells (EPCs) under a local condition. The purpose of this study was to evaluate the late effects of IPC on endothelial function in smokers.. Methods and Results: Late phase of IPC was induced by upper limb ischemia (cuff inflation of over 200 mmHg for 5 minutes) six times a day for one month. We evaluated forearm blood flow (FBF) responses to acetylcholine (ACh) and to sodium nitroprusside (SNP) before and after IPC stimulus in 15 male smokers (27±7 yr) and 15 male non-smokers (26±5 yr). FBF was measured using a strain-gauge plethysmography. The IPC stimulus significantly increased plasma ...
Endothelial cells line the inner walls of all the arteries, where they release substances that can cause vasodilation and lower the blood pressure. The loss of endothelium-dependent vasodilation increases vascular resistance and blood pressure in cardiovascular disorders. Thus, strategies to target the loss of endothelium-dependent vasodilation may have therapeutic benefit in cardiovascular disorders.. Under normal conditions, endothelium-dependent vasodilation is driven by increases in intracellular calcium. My laboratory studies the activity of individual calcium entry events in endothelial cells and their signaling targets under normal and disease conditions. We focus on two life-threatening disorders that are commonly associated with the loss of endothelial function- obesity and pulmonary hypertension. New findings reveal that calcium influx through TRPV4 ion channels, a key calcium entry pathway in endothelial cells, is drastically reduced in rodent models of obesity or pulmonary ...
The purpose of this study was to investigate the effect of race and subclinical elevations in blood pressure (i.e., prehypertension) on cutaneous sensory nerve-mediated and nitric oxide (NO)-dependent vasodilation. We recruited participants who self-identified as either non-Hispanic black (n = 16) or non-Hispanic white (n = 16). Within each group, participants were subdivided as either normotensive (n = 8 per group) or prehypertensive (n = 8 per group). Each participant was instrumented with four intradermal microdialysis fibers: 1) control (lactated Ringers), 2) 5% lidocaine (sensory nerve inhibition), 3) 20 mM Nω-nitro-l-arginine methyl ester (l-NAME) (NO synthase inhibition), and 4) lidocaine + l-NAME. Skin blood flow was assessed via laser-Doppler flowmetry, and each site underwent local heating from 33°C to 39°C. At the plateau, 20 mM l-NAME were infused at control and lidocaine sites to quantify NO-dependent vasodilation. Maximal vasodilation was induced via 54 mM sodium nitroprusside ...
Synonyms for vasodilation in Free Thesaurus. Antonyms for vasodilation. 2 words related to vasodilation: dilatation, dilation. What are synonyms for vasodilation?
In rat cremasteric microcirculation, mechanical occlusion of one branch of an arteriolar bifurcation causes an increase in flow and vasodilation of the unoccluded daughter branch. This dilation has been attributed to the operation of a shear stress-dependent mechanism in the microcirculation. Instead of or in addition to this, we hypothesized that the dilation observed during occlusion is the result of a conducted signal originating distal to the occlusion. To test this hypothesis, we blocked the ascending spread of conducted vasomotor responses by damaging the smooth muscle and endothelial cells in a 200-microm segment of second- or third-order arterioles. We found that a conduction blockade eliminated or diminished the occlusion-associated increase in flow through the unoccluded branch and abolished or strongly attenuated the vasodilatory response in both vessels at the branch. We also noted that vasodilations induced by ACh (10(-4) M, 0.6 s) spread to, but not beyond, the area of damage. Taken
Percent change in coronary blood flow, coronary vascular resistance and coronary epicardial diameter in response to (A) endothelium-dependent vasodilation with acetylcholine and (B) endothelium-independent vasodilation with sodium nitroprusside. (C) Percent change in coronary blood flow and coronary vascular resistance in response to adenosine. Overweight and obese subjects (BMI ≥ 25 kg/m2) in dark columns and normal weight subjects (BMI , 25kg/m2) in open columns. Results expressed as mean ± SEM. Probability values by students t-test ...
This study aimed to examine the effects of aerobic training on endothelium-dependent vasorelaxation induced by acetylcholine and the expression of enzymes controlling NO bioavailability in the aorta of hypertensive rats.. We confirmed findings from previous reports showing that compared with the WKYsd group, the SHRsd group exhibits higher BP and impaired maximal vasorelaxation 24,25. Moreover, the relative endothelium-dependent vasorelaxation induced by 10-4 M ACh was lower in the SHRsd group than in WKY and showed paradoxical vasoconstriction in SHR. These results clearly reveal endothelial dysfunction in the aorta of SHR 24,32. Acetylcholine activates smooth muscle muscarinic receptors and evokes endothelium-dependent contractions in the aortas of SHR, but not WKY 33.. When aorta samples were incubated with L-NAME, differences in maximal vasorelaxation were not observed, but the relative endothelium-dependent vasorelaxation induced by ACh (10-4 M) remained different between the SHRsd and ...
To test the hypothesis that activation of protein kinase C impairs vascular reactivity in patients with diabetes.. A major cause of death and disability in patients with diabetes mellitus is atherosclerosis. Endothelial dysfunction is an important, if not primary, factor in atherogenesis. Nitric oxide is an important substance made and released by the endothelium. Many prior studies in animals and humans have shown that the ability of the blood vessel to dilate is impaired in diabetes. This process of vasodilation is mediated by a substance, nitric oxide, which is thought to be highly susceptible to destruction by oxidant molecules. In previous studies, we found that acute administration of the antioxidant, vitamin C, improves endothelium-dependent vasodilation in blood vessels of patients with type 1 and type 2 diabetes. This suggests that by scavenging oxidants, such as superoxide, vitamin C may reduce the destruction of nitric oxide and thereby preserve endothelial function. Additional ...
DNA damage is an important contributor to endothelial dysfunction and age-related vascular disease. Recently, we demonstrated in a DNA repair-deficient, prematurely aging mouse model (Ercc1Δ/− mice) that dietary restriction (DR) strongly increases life- and health span, including ameliorating endothelial dysfunction, by preserving genomic integrity. In this mouse mutant displaying prominent accelerated, age-dependent endothelial dysfunction we investigated the signaling pathways involved in improved endothelium-mediated vasodilation by DR, and explore the potential role of the renin-angiotensin system (RAS). Ercc1Δ/− mice showed increased blood pressure and decreased aortic relaxations to acetylcholine (ACh) in organ bath experiments. Nitric oxide (NO) signaling and phospho-Ser1177-eNOS were compromised in Ercc1Δ/−. DR improved relaxations by increasing prostaglandin-mediated responses. Increase of cyclo-oxygenase 2 and decrease of phosphodiesterase 4B were identified as potential ...
Cardiovascular dysfunction is usually a primary indie predictor of age-related morbidity and mortality. Strategies To be able to evaluate the function of IL-10 in maintenance of vascular function, power stress myography was useful to gain access to ex-vivo endothelium reliant vasorelaxation in vessels isolated from IL-10 knockout IL-10(tm/tm) and control mice. Pulse influx speed ((PWV), index of rigidity) of vasculature was assessed using ultrasound and blood circulation pressure was assessed using the tail cuff technique. Echocardiography was utilized to elucidated framework and functional adjustments in the center. Outcomes Mean arterial stresses were considerably higher in IL-10(tm/tm) mice when compared with C57BL6/outrageous type (WT) handles. PWV was elevated in IL-10(tm/tm) indicating stiffer vasculature. GMCSF Endothelial unchanged aortic bands isolated from IL-10(tm/tm) mice confirmed impaired vasodilation at low acetylcholine dosages and vasoconstriction at higher dosages whereas ...
1 l-arginine supplement - l-arginine exposed!, #1 l-arginine supplement - l arginine exposed! find out how l-arginine will help you. free shipping for limited time. stocks are running out fast!. L-arginine as a nutritional prophylaxis against vascular, Reduced substrate may be rate limiting and reduce no formation and subsequently endothelial-dependent vasodilation. l-arginine (2-amino-5-guanidinovaleric acid) is a ...
This medical exhibit provides an overview of the venous circulatory system. It also illustrates the process of vasodilation and subsquent shock.
MOA: AT1-receptor antagonists. Block the activation of angiotensin II AT1 receptor on vessels which directly causes vasodilatation, reduces secretion of vasopressin, reduces production and secretion of ...
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
Wicked is a new and exciting formula which contains high amounts of stimulants, compounds to enhance focus and boost vasodilation and muscular pumps in one! Predator Nutrition
The principal finding of this study is that IC inhibits NO-mediated endothelium-dependent and -independent vasodilation in rat aortic vascular smooth muscle. IC inhibited both receptor- and non-receptor-mediated endothelium-dependent vasodilation induced by ACh, histamine, and A23187 and endothelium-independent vasodilation induced by SNP. Agents like ACh, histamine, and A23187 produce vasodilation through the endothelial synthesis and release of NO, which activates vascular smooth muscle soluble guanylyl cyclase to produce an increase of cGMP concentration.15 16 19 SNP produces vasodilation by activation of soluble guanylyl cyclase after its breakdown to NO.24 Thus, the site of action for NO is soluble guanylyl cyclase, whether it is released endogenously from endothelial cell activation by receptor-mediated (ACh, histamine) or non-receptor-mediated (A23187) agents or is produced intracellularly in the smooth muscle cells from metabolism of the nitrovasodilator SNP.24 Our findings that IC had ...
In the present article we report that deletion polymorphism in the ACE gene is associated with an impairment of endothelium-dependent vasodilation in a group of newly discovered, never-treated hypertensive patients. Our patients who were homozygous for deletion (DD) are characterized by significantly less endothelium-dependent vasodilation compared with subjects who were homozygous for insertion (II) and heterozygous (ID). Furthermore, the present data demonstrate that normotensive controls with a DD genotype had similar endothelium-dependent vascular responses when compared with these normotensive individuals with the non-DD genotype. Similarly, although the DD genotype among hypertensive patients was associated with further impairment of endothelium-dependent vasodilation, it must be noted that hypertensive patients with the non-DD genotype also had significantly impaired endothelium responses compared with normotensive controls. Thus, it is clear that it is hypertension and not the ACE ...
HIV-infected subjects on a stable protease inhibitor (PI) containing antiretroviral regimen with plasma HIV RNA ,500 copies/mL, who have LDL cholesterol levels ,130 mg/dL or fasting triglycerides levels ,200 mg/dL, will be randomized (1:1) to continue their current antiretroviral regimen or to switch the PI to atazanavir (ATV). Brachial artery reactivity will be measured before (at entry) and 12 and 24 weeks after subjects are randomized.. ARM A: Switch current PI to atazanavir 400 mg once daily plus current , 2 nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) for 24 weeks.. Subjects currently on ritonavir (RTV) (400 mg BID or greater) or RTV-boosted PI (,400 mg/day) , or tenofovir (TDF) as backbone NRTI therapy, will switch to ATV 300 mg boosted with RTV 100mg once daily.. ARM B: Continue current antiretroviral regimen (single or RTV-boosted PI plus , 2 NRTIs) for 24 weeks. Brachial artery reactivity in response to two vasoactive stimuli (increased forearm blood flow and ...
BACKGROUND: Some studies have demonstrated beneficial effects of L-arginine as a substrate for nitric oxide synthesis, and diclofenac as an inhibitor of cyclooxygenase (COX)-derived vasoconstrictive agents on vascular responses in humans during several pathological conditions. The aim of the present study was to investigate the acute effects of L-arginine and diclofenac on endothelium-dependent vasodilatation (EDV) and endothelium-independent vasodilatation (EIDV) in patients with chronic renal failure (CRF).. METHODS: Effects of L-arginine and diclofenac on EDV and EIDV were measured in 15 patients with CRF and in 15 healthy controls by means of forearm blood flow measurements with venous occlusion plethysmography during local intra-arterial infusions of methacholine (2 and 4 micro g/min evaluating EDV) and sodium nitroprusside (5 and 10 micro g/min evaluating EIDV).. RESULTS: L-Arginine infusion increased methacholine-induced vasodilatation both in patients with CRF and healthy controls. ...
The findings of the present study show that endothelium-dependent vasodilation was preserved in young untreated subjects with BH, in whom their BP elevation had persisted over a period of 4 to 5 years. However, BH subjects had a nonspecific attenuation of the vasodilatory response to the NO donor SNP. The observation that the relative vascular response to MCh over SNP was even greater in BH subjects supports the interpretation that the reduced FBF response was not due to a dysfunction of the endothelium per se. Rather, it appears that the functional impairment of the vasorelaxant response may be related to some as-yet-undefined ineffective action of NO on the vascular smooth muscle cells or to structural changes in the vasculature. To test this hypothesis, we also investigated the postischemic vasodilatory capacity, which may reflect structural vascular changes and/or reduced production or action of endogenous vasodilator release during tissue ischemia. However, BH subjects had no evidence of ...
BACKGROUND: While recent reports suggest that both flow-mediated vasodilation (FMD) in the brachial artery (BA), endothelium-dependent vasodilatation, and intima media thickness (IMT) in the carotid artery correlate with the extent of coronary artery
BACKGROUND Impaired arterial dilatation response to nitroglycerin has been observed in adults with risk factors for atherosclerosis and in patients with established atherosclerotic disease. This defect parallels changes in vascular endothelial function and may be attributed to increased oxidative stress. Because atherosclerosis begins in childhood, we examined the correlates of nitrate-mediated dilatation (NMD) in children, including brachial artery endothelial function, oxidized LDL, and carotid artery intima-media thickness (IMT). METHODS AND RESULTS Brachial artery flow-mediated endothelium-dependent dilatation (FMD) and nitrate-mediated smooth muscle function, IMT of the carotid bulb, and brachial artery and oxidized LDL were measured in 142 children (mean age, 11 years; range, 8 to 17 years), including 87 healthy children, 41 diabetic children, and 14 children with familial hypercholesterolemia. NMD correlated directly with FMD (r=0.46, P|0.001) and inversely with brachial artery baseline
TY - JOUR. T1 - The Flow-mediated Dilation Response to Acute Exercise in Overweight Active and Inactive Men. AU - Harris, Ryan. AU - Padilla, Jaume. AU - Hanlon, Kevin P. AU - Rink, Lawrence D. AU - Wallace, Janet P. N1 - Reference text: 1. Eckel RH, Krauss RM. American Heart Association call to action: obesity as a major risk factor for coronary heart disease. Circulation 1998;97:2099-2100. 2. Lusis AJ. Atherosclerosis. Nature 2000;407:233-241. 3. Ross R. The pathogenesis of atherosclerosis-an update. N Engl J Med 1986;314:488-500. 4. Munro JM, Cotran RS. The pathogenesis of atherosclerosis: atherogenesis and inflammation. Lab Invest 1988;58:249-261. 5. Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB. Elevated C-reactive protein levels in overweight and obese adults. JAMA 1999;282:2131-2135. 6. Blair SN, Kohl HW 3rd, Paffenbarger RS Jr et al. Physical fitness and all cause mortality. A prospective study of healthy men and women. JAMA 1989;262:2395-2401. 7. Lee CD, Blair SN, Jackson AS. ...
TY - JOUR. T1 - Endothelium-derived hyperpolarizing factor(s). T2 - Species and tissue heterogeneity. AU - Triggle, C. R.. AU - Dong, H.. AU - Waldron, G. J.. AU - Cole, W. C.. PY - 1999/1/1. Y1 - 1999/1/1. N2 - 1. Endothelium-derivcd relaxing factor is almost universally considered to be synonymous with nitric oxide (NO); however, it is now well established that at least two other chemically distinct species (prostacyclin (PGI2) and a hyperpolarizing factor) may also contribute to endothelium-dependent relaxation. 2. Only relatively few studies have provided definitive evidence that an endothelium-derived hyperpolarizing factor (EDHF), which is neither NO nor PGI2, exists as a chemical mediator. 3. There is a lack of agreement as to the likely chemical identity of this putative factor. Some evidence suggests that EDHF may be a cytochrome P450-derived arachidonic acid product, possibly an epoxyeicosatrienoic acid (EET); conflict-ing evidence supports an endogenous cannabinoid as the mediator and ...
Markus Juonala;Costan G. Magnussen;Alison Venn;Seana Gall;Mika Kähönen;Tomi Laitinen;Leena Taittonen;Terho Lehtimäki;Eero Jokinen;Cong Sun;Jorma S.A. Viikari;Terence Dwyer;Olli T. Raitakari ...
Flow-mediated, endothelium-dependent vasodilation in response to transient arterial occlusion was determined with ultrasonographic imaging of the brachial artery with an 11 MHz linear array ultrasound transducer connected to an ATL Apogee 800 plus duplex ultrasound machine (Advanced Technology Laboratories, Bothell, Washington) adapted from previously published methods (15,16). The axial resolution of the 11 MHz transducer is capable of detection of changes in brachial artery diameter of ,0.1 mm. Arterial diameter (cm) was determined as the internal dimension of the vessel wall, from trailing edge to leading edge of the anterior and posterior intimal markings, respectively (to confirm full alignment of the ultrasound beam with the maximum anterior-posterior diameter of the brachial artery in its long axis). Brachial artery blood flow velocity was determined with a 1.2 mm pulsed Doppler ultrasound sampling volume placed in the center of the image of the vessel lumen with internal software ...
The proposed mechanistic link between the age-related attenuation in vascular function and free radicals is an attractive hypothesis; however, direct evidence of free radical attenuation and a concomitant improvement in vascular function in the elderly is lacking. Therefore, this study sought to test the hypothesis that ascorbic acid (AA), administered intra-arterially during progressive handgrip exercise, improves brachial artery (BA) vasodilation in a nitric oxide (NO)-dependent manner, by mitigating free radical production. BA vasodilation (Doppler ultrasound) and free radical outflow [electron paramagnetic resonance (EPR) spectroscopy] were measured in seven healthy older adults (69 ± 2 yr) during handgrip exercise at 3, 6, 9, and 12 kg (∼13-52% of maximal voluntary contraction) during the control condition and nitric oxide synthase (NOS) inhibition via N(G)-monomethyl-L-arginine (L-NMMA), AA, and coinfusion of l-NMMA + AA. Baseline BA diameter was not altered by any of the treatments, while L
TY - JOUR. T1 - Effect of cigar smoking on endothelium-dependent brachial artery dilation in healthy young adults. AU - Santo-Tomas, Minerva. AU - Lopez-Jimenez, Francisco. AU - Machado, Humberto. AU - Aldrich, Harry R.. AU - Lamas, Gervasio A.. AU - Lieberman, Eric H.. PY - 2002. Y1 - 2002. N2 - Background: Cigar smoking has become a quickly growing trend among teenagers, women, and young adults. The objective was to explore whether cigar smoking affects flow-mediated vasodilation in healthy, non-smoking young adults. Methods: This was a prospective randomized trial with open design. It was performed in a cardiology teaching program in a private community hospital that serves as a major referral center within the greater Miami area. Apparently healthy, non-smoking young adult cardiology trainees and staff between the ages of 20 and 45 years were randomly assigned to a cigar smoking group (n = 15) or a control group (n = 14). The main outcome measures were the difference in percent diameter ...
Looking for cold-induced vasodilation? Find out information about cold-induced vasodilation. A sequence of vasoconstriction followed by vasodilation that acts as a protective mechanism to prevent cold weather injury to the extremities Explanation of cold-induced vasodilation
Vascular ultrasound is a specialist form of diagnostic imaging involving the study of the peripheral vascular system and its diseases including peripheral arterial disease, chronic venous disease (varicose veins), and acute venous disease (deep vein thrombosis). Performing vascular ultrasound scans requires expertise in B-mode, colour Doppler, and pulse wave Doppler modalities coupled with a sound knowledge of vascular anotomy, haemodynamics, vascular disease, and both endovascular and surgical vascular procedures.. South East Vascular Ultrasound has been providing a dedicated specialist vascular imaging service to the south eastern suburbs for over 14 years with locations in Richmond (The Epworth Centre), Blackburn, Waverley, and Bentleigh. The senior sonographer is Stephen Wood who has over 20 years experience as a dedicated vascular sonographer.. South East Vascular Ultrasound is fully accredited under the Australian Government Department of Healths Diagnostic Imaging Accreditation Scheme. ...
This study demonstrated that treatment with a single dose of commonly used antihypertensive and antianginal medication lowers blood pressure and heart rate, but has no effect on resting brachial artery size, FMD, NMD, and the reproducibility of FMD. These results were obtained when healthy patients received single doses of specific agents for the first time and when patients on chronic therapy for CAD are studied before and after receiving their clinically prescribed medications. These findings suggest that acute alterations in systemic hemodynamics and/or local resting arterial tone induced by these medications do not alter the capacity of the brachial artery to respond to endothelium-derived and exogenous vasodilators.. No previous study examined the specific question addressed in the current study. In most prior studies of endothelial function in human subjects, all vasoactive medications were withheld for at least 24 h, and a recent paper recommended withholding medications for four ...
We fed 10 healthy, normolipidemic subjects five meals containing 900 kcal and 50 g fat. Three meals contained different fat sources: olive oil, canola oil, and salmon. Two olive oil meals also contained antioxidant vitamins (C and E) or foods (balsamic vinegar and salad). We measured serum lipoproteins and glucose and brachial artery flow-mediated vasodilation (FMD), an index of endothelial function, before and 3 h after each meal ...
The purpose of this study was to determine the association between vascular diameters and amount of magnification and to assess the influence of the magnification media on the microanastomosis quality and permeability. Sixty arterial microanostomoses
Vasodilation is where blood vessels widen.[1] It results from relaxation of muscle cells within blood vessel walls. The process is essentially the opposite of vasoconstriction, which is the narrowing of blood vessels.. When vessels widen, blood flow is increased. This in turn decreases blood pressure. Drugs that cause vasodilation are called vasodilators.. ...
The aim of this study was to determine whether there is an age-related decline in vascular responsiveness to bradykinin, whose vasodilatory action is mediated chiefly through endothelium-derived relaxing factor (EDRF). Dose-response curves for bradykinin were constructed using the dorsal hand vein compliance technique in veins preconstricted with phenylephrine in 27 volunteers (16 male, 11 female) aged 18 to 81 years. At the end of the bradykinin study, 12 subjects had a single infusion of a high dose of isoproterenol. There was no correlation between age and the EMAX or the log ED50 for bradykinin, although the same subjects showed a correlation between age and EMAX for isoproterenol, as previously found. There was no significant difference in either the EMAX or the log ED50 between male and female subjects. The results suggest that bradykinin-induced vasodilation is independent of age or gender.
Nicotinic acid, known as vitamin B3, is an effective lipid lowering drug and intense cutaneous vasodilator. This study reports the effect of 2-(1-adamantylthio)nicotinic acid (6) and its amide 7 and nitrile analog 8 on phenylephrine-induced contraction of rat thoracic aorta as well as antioxidative activity. It was found that the tested thionicotinic acid analogs 6-8 exerted maximal vasorelaxation in a dose-dependent manner, but their effects were less than acetylcholine (ACh)-induced nitric oxide (NO) vasorelaxation. The vasorelaxations were reduced, apparently, in both NG-nitro-L-arginine methyl ester (L-NAME) and indomethacin (INDO). Synergistic effects were observed in the presence of L-NAME plus INDO, leading to loss of vasorelaxation of both the ACh and the tested nicotinic acids. Complete loss of the vasorelaxation was noted under removal of endothelial cells. This infers that the vasorelaxations are mediated partially by endothelium-induced NO and prostacyclin. The thionicotinic acid analogs all
Fingerprint Dive into the research topics of Inhibition of renin-angiotensin system reverses endothelial dysfunction and oxidative stress in estrogen deficient rats. Together they form a unique fingerprint. ...
TY - JOUR. T1 - The impact of caffeine on vasodilator stress perfusion studies. AU - Lapeyre, Andre C.. AU - Goraya, Tauqir Y.. AU - Johnston, Donald L.. AU - Gibbons, Raymond J.. PY - 2004/1/1. Y1 - 2004/1/1. UR - UR - U2 - 10.1016/j.nuclcard.2004.04.003. DO - 10.1016/j.nuclcard.2004.04.003. M3 - Article. C2 - 15295419. AN - SCOPUS:4243134949. VL - 11. SP - 506. EP - 511. JO - Journal of Nuclear Cardiology. JF - Journal of Nuclear Cardiology. SN - 1071-3581. IS - 4. ER - ...
TY - JOUR. T1 - Role of angiotensin II and α-adrenergic receptors during estrogen-induced vasodilation in ewes. AU - Davis, L. E.. AU - Magness, R. R.. AU - Rosenfeld, C. R.. PY - 1992/1/1. Y1 - 1992/1/1. N2 - Estradiol-17β (E2β) produces uterine and systemic vasodilation in nonpregnant ewes without altering mean arterial pressure (MAP). Mechanisms responsible for maintaining MAP and thus uterine blood flow (UBF) may include activation of the renin-angiotensin and/or adrenergic systems. We therefore investigated the effects of systemic blockade of angiotensin II (ANG II) and/or α-adrenergic receptors in nonpregnant, castrated ewes, using saralasin (Sar) and/or phentolamine (Phen) in the presence or absence of intravenous E2β (1.0 μg/kg). In nonestrogenized ewes neither antagonist alone had substantial cardiovascular effects; however, Sar + Phen decreased systemic vascular resistance (SVR) 20 ± 7.4% (SE) and increased heart rate (HR) 50 ± 19% (P , 0.01); MAP and UBF were unaffected. ...
Although we found that the vasoconstrictor response to l-NMMA was lower in blacks, we did not examine effects of other nonspecific vasoconstrictors to investigate whether this is a reflection of reduced sensitivity of the vascular smooth muscle to vasoconstrictors. However, the fact that the constrictor response to TEA was similar to whites suggests that the response to l-NMMA is specific for reduced NO bioavailability. The reduced sensitivity to exogenous NO (sodium nitroprusside) complicates the interpretation of the reduced dilator responses observed with acetylcholine and bradykinin in blacks. However, because basal NO and the contribution of NO during exercise is lower in blacks, it is likely that in addition to reduced sensitivity, there is also an endothelial defect in NO release in blacks.. l-NMMA and TEA are competitive inhibitors, and thus our results may underestimate the physiological contribution of both NO and K+Ca channels to vasodilation. Our investigation was conducted on a ...
The purpose of this study was to investigate if myogenic responses of isolated coronary arterioles were dependent on an intact, functional endothelium. Arterioles were located in situ by intracoronary perfusion with india ink-gelatin solution and then dissected and cannulated at both ends with glass micropipettes. Intraluminal pressure was initially set at 60 cm H2O; then the pressure was altered in steps of 20 cm H2O over a range of 20-140 cm H2O. Arterioles developed spontaneous tone and exhibited a significant myogenic response in physiological saline solution (36 degrees -37 degrees C). Arteriolar dilation and constriction were observed at lower (20-60 cm H2O) and higher (60-140 cm H2O) pressures, respectively. The presence of a functional and automatically intact endothelium was confirmed by relaxation to the endothelium-dependent vasodilator bradykinin and by transmission electron microscopy, respectively. After mechanical denudation of the endothelium with a specially designed abrasive ...
Forty-seven papers on the mechanisms whereby natural regulatory phenomena and synthetic vasodilator agents effect vasodilation. Outlines the complexity of the physiologic regulation of vascular smooth muscle tone and provides different points of view on debated issues. From a symposium, Mechanisms of Vasodilation, held July 1980 in Belgium. Five sections: neurohumoral regulation, local regulation, cellular mechanisms, the blood-vessel wall in hypertension, and vasodilator agents. ...
Background Premenopausal women have a lower incidence of cardiovascular disease, which may partly be due to a protective effect of estrogen on endothelial function. Animal studies suggest that estrogen may also improve the relationship between shear rate ( SR ) and endothelial function. We aimed to explore the relationship between endothelial function (ie, flow-mediated dilation [ FMD ]) and SR (ie, SR area under the curve [ SRAUC ]) in women versus men, and between pre- versus postmenopausal women. Methods and Results Brachial artery FMD and SRAUC were measured in accordance with expert-consensus guidelines in 932 healthy participants who were stratified into young adults (18-40 years, 389 men, 144 women) and older adults (,40 years, 260 men, 139 women). Second, we compared premenopausal (n=173) and postmenopausal women (n=110). There was evidence of a weak correlation between SRAUC and FMD in all groups but older men, although there was variation in strength of outcomes. Further exploration ...
We found that Nrf2 KO mice show an impaired left ventricular diastolic function as assessed by high resolution ultrasound. Accordingly, isolated perfused Nrf2 KO hearts showed an impaired response to β adrenergic stimulation by isoproterenol, while systolic left ventricular function was preserved. Surprisingly, blood pressure in Nrf2 KO mice was significantly decreased, and endothelial function of arterial conductance and coronary resistive vessels was preserved. This is consistent with an increased maximal dilation after vascular occlusion of the arteria iliaca externa, which indicates a fully preserved vascular and endothelial function in these mice. Mice lacking the endothelial nitric oxide synthase (eNOS KO) showed no dilatatory response to shear stress, confirming that flow-mediated-dilation response mainly depends on eNOS-dependent vasodilatory pathways. The circulating NO pool analysed by HPLC and chemiluminescence showed no differences between Nrf2 KO mice and WT littermates. However, ...
In the current study, we found that type 2 diabetes impaired the ability of mesenteric arteries to remodel and improve NO-dependent dilation in response to a chronic increase in blood flow. Indeed, AGEs and RAGEs were overexpressed, whereas eNOS level and MMP activity were reduced in arteries from ZDF rats. Ongoing treatment with the AGE-breaker ALT-711 restored the ability of mesenteric arteries from ZDF rats to increase their diameter and improved endothelium-dependent dilation in response to a chronic rise in blood flow.. Physiologically, a chronic rise in blood flow in resistance arteries enlarges vascular diameter and improves endothelium-dependent dilation (9,19,34). This remodeling is essential to adjust organ perfusion during physiological processes, such as development (35), pregnancy (36), or exercise training (37), as well as during pathological processes (mainly ischemic diseases). A similar remodeling also occurs in response to vasodilator treatments (38,39). This remodeling plays a ...
Introduction to Peripheral Vascular Ultrasound Online Course is designed to provide a comprehensive introduction to peripheral vascular sonography and has been designed to provide a strong foundation to perform and/or interpret vascular ultrasound examinations.
Endothelium plays a critical role in maintaining healthy homeostatic properties of the vasculature. Endothelial dysfunction promotes atherosclerosis by creating a vasospastic, prothrombotic, and proinflammatory milieu. Therefore, the assessment of endothelial function as a surrogate marker of arterial health has gained significant interest for clinical risk assessment beyond the risk conveyed by a structural impediment to flow (1). Furthermore, the observation that cardiovascular events may occur remotely from the site in which the endothelial dysfunction is detected prompted clinical studies in search for peripheral vascular endothelial dysfunction as a predictor of cardiovascular events.. Endothelial dysfunction is characterized by a paradoxical vasoconstriction or attenuated dilation due to reduced endothelium-dependent nitric oxide (NO) release. In earlier studies, the response of the epicardial arteries to infused acetylcholine was measured invasively to assess endothelial function in the ...
With the worlds elderly population expected to double by 2050, understanding how aging affects the body is an important focus for researchers globally. Cardiovascular disease, the No. 1 cause of death worldwide, often is associated with aging arteries that restrict blood flow. Now, University of Missouri researchers have identified an age-related cause of arterial dysfunction, a finding that could lead to future treatments for some forms of vascular disease., With the worlds elderly population expected to double by 2050, understanding how aging affects the body is an important focus for researchers globally. Cardiovascular disease, the No. 1 cause of death worldwide, often is associated with aging arteries that restrict blood flow. Now, University of Missouri researchers have identified an age-related cause of arterial dysfunction, a finding that could lead to future treatments for some forms of vascular disease.
OBJECTIVE: To search for determinants of endothelial dysfunction in type 2 diabetes. RESEARCH DESIGN AND METHODS: We performed a comprehensive analysis of cardiovascular risk markers and measured blood flow responses to endothelium-dependent (acetylcholine [ACh] and NG-monomethyl-L-arginine) and -independent (sodium nitroprusside [SNP]) vasoactive agents in 30 nonsmoking men with type 2 diabetes (age 51 +/- 1 years, BMI 27.8 +/- 0.4 kg/m2, HbA1c 7.4 +/- 0.3%) and 12 matched normal control men. RESULTS: ACh-induced vasodilation was 37% lower in type 2 diabetic (6.1 +/- 0.5) than in normal subjects (9.7 +/- 1.5 ml.dl-1.min-1, P , 0.01), while flows during SNP were similar (9.1 +/- 0.6 vs. 9.9 +/- 1.3 ml.dl-1.min-1, NS). The ratio of endothelium-dependent vs. -independent flow (ACh:SNP ratio) was 31% lower in type 2 diabetic (0.70 +/- 0.05) than in normal subjects (1.10 +/- 0.18, P , 0.01). Total (2.2 +/- 0.4 vs. 1.3 +/- 0.2 mmol/l, P , 0.05), VLDL, and intermediate-density lipoprotein ...
In the present study, the role of reactive oxygen species and the contribution of antioxidant defence in the time course of changes in acetylcholine-stimulated endothelium-dependent and sodium nitroprusside-stimulated endothelium-independent relaxation were investigated in aortic rings isolated from 6-month streptozotocin-diabetic and age-matched control rats. Although there were no significant differences in the degree of the peak relaxations produced by a single administration of acetylcholine (1 μM) or sodium nitroprusside (0.01 μM) between control and diabetic rings, the endothelium-dependent and -independent relaxant responses were more transient and the time required to reach a peak relaxation after addition of acetylcholine was shorter in diabetic vessels. Pretreatment of diabetic vessels with superoxide dismutase (100 U/ml) normalized the recovery phases of endothelium-dependent and -independent relaxations, but had no effect on the peak responses to acetylcholine and sodium ...
Did you know that dark circles under your eyes are a result of the influence of histamine on vasodilation. Histamines dilate blood vessels (vasodilate). So if you are having an allergic reaction that is filling up your histamine bucket, you probably have dark circles under your eyes. I can attest to this. Ever since I…
Vasodilation[edit]. The bulbar conjunctival microvasculature is known to dilate in response to several stimuli and external ... Bulbar conjunctival vasodilation has also been shown to correlate changes in emotional state.[33] ...
VasodilationEdit. Substance P is a potent vasodilator. Substance P-induced vasodilatation is dependent on nitric oxide release. ... "In vivo measurement of endothelium-dependent vasodilation with substance P in man". Herz. 17 (5): 284-90. PMID 1282120.. ...
Vasoconstriction and vasodilationEdit. Immediately after a blood vessel is breached, ruptured cell membranes release ... The main factor involved in causing vasodilation is histamine.[3][15] Histamine also causes blood vessels to become porous, ... Latent period: During the haemostatic and inflammatory phase of the wound healing process, vasodilation and permeabilisation ... This vasoconstriction lasts five to ten minutes and is followed by vasodilation, a widening of blood vessels, which peaks at ...
... which inhibits it and leads to smooth muscle relaxation and vasodilation. It can be noted that PGI2 and TXA2 work as ...
cutaneous vasodilation. [3] Clinically the most significant feature is delirium, particularly in the elderly, who are most ...
possible vasodilation. Nociceptin receptor NOR. OP4 (I). ORL1. *brain *cortex ...
vasodilation, inhibits platelets and pro-inflammatory cells. role(s) in human disease not yet proven[76][77] ... Many of the prostanoids are known to mediate local symptoms of inflammation: vasoconstriction or vasodilation, coagulation, ...
Arteriolar vasodilation occurs. The smooth muscle walls of the arterioles relax allowing increased blood flow through the ...
"Vasodilation and Vasoconstriction: Real Story." Vasodilation and Vasoconstriction. 2011. Web. 21 May 2012. University of ... Vasodilation is, in essence, the opposite of vasoconstriction. In vasodilation the blood vessels dilate to allow more blood ... Like vasoconstriction, vasodilation can be caused by internal and external factors. For example, nitric oxide, found in food, ... Vasodilation is also triggered for thermoregulation to provide heat dissipation. The Starling Equation describes the flow of a ...
Through their role in vasodilation, prostaglandins are also involved in inflammation. They are synthesized in the walls of ...
vasodilation. secretory cells (mostly). ↑secretion (vesicle fusion). juxtaglomerular cell. ↓secretion[14]. Parathyroid chief ...
Chemoreceptors are responsible for signaling vasoconstriction, vasodilation, bronchoconstriction, and bronchodilation.[citation ...
Vasodilation and vasoconstriction are also used antagonistically as methods of thermoregulation. Vasoconstriction is the ... Vasodilation is a similar process mediated by antagonistically acting mediators. The most prominent vasodilator is nitric oxide ...
The bark, wood, and seeds contain coumarin.[16][17] They have anti-inflammatory, sedative and vasodilation effects. ...
In higher concentrations it causes endothelium-independent vasodilation and has a negative inotropic effect on cardiac output ... Endogenous sulfur dioxide in low concentrations causes endothelium-dependent vasodilation. ...
Vasodilation. References[edit]. *^ Fuster, V.; Alexander, R.W.; O'Rourke, R.A. (2004) Hurst's the heart, book 1. 11th Edition, ... Because adenosine acts as a direct vasodilator, it is not dependent on an intact endothelium to cause vasodilation. ... Adenosine causes vasodilation in the small and medium-sized resistance arterioles (less than 100 µm in diameter). When ... However, it causes vasodilation and decreased vascular resistance during hypoxia. Adenosine is formed in the myocardial cells ...
Maruhashi, T; Kihara, Y; Higashi, Y (2018). "Assessment of endothelium-independent vasodilation: From methodology to clinical ...
Additional side effects include low blood pressure related to vasodilation, transient apnea following induction doses, and ... 1997). "Mechanisms whereby propofol mediates peripheral vasodilation in humans (1997)". Anesthesiology. 86 (1): 64-72. doi: ... possibly through direct vasodilation.[46] There are also reports that it may cause green discolouration of the urine.[47] ...
This is called vasodilation.) This helps make the blood pressure lower. It also makes the skin warmer, and can cause a man to ...
Through their role in vasodilation, prostacyclins are also involved in inflammation. They are synthesized in the walls of blood ...
CO acts as a cellular messenger and functions in vasodilation.[29] ...
The mechanisms of vasodilation are predominantly local metabolites and myogenic effects. Increased metabolic activity of the ... These changes cause significant vasodilation. The reverse occurs when metabolic activity is slowed and these substances wash ... These vasodilators released from the tissue act on local arterioles causing vasodilation, this causes a decrease in vascular ... this then elicits arteriolar vasodilation consequently, creating a pathway of least resistance so blood flow can be precisely ...
Another theory about the cause of HACE is that hypoxia may induce nitrous oxide synthase.[24] Vasodilation is caused by the ...
In most tissues of the body, the response to hypoxia is vasodilation. By widening the blood vessels, the tissue allows greater ...
Under hypoxic conditions, nitrite may release nitric oxide, which causes potent vasodilation. Several mechanisms for nitrite ...
The process is the opposite of vasodilation, the widening of blood vessels. The process is particularly important in ...
"Arachidonic acid-induced vasodilation of rat small mesenteric arteries is lipoxygenase-dependent". Journal of Pharmacology and ...
Both of these factors affect pH and, in turn, the balance between vasodilation versus vasoconstriction in the brain. So, the ... In response to the blood flow interruption, a temporary compensatory vasodilation occurs as soon as blood flow has resumed, ... Vasodilation Vasoconstriction Vascular resistance "CV Physiology , Local Regulation of Blood Flow". ... While nitric oxide causes vasodilation, endothelin-1 causes vasoconstriction. Below are several examples of differing types of ...
This causes vasodilation and improves hemodynamics. DATS is a promising treatment for cardiac arrhythmias through its ability ...
Vasodilation and vasoconstriction are complex phenomena; they are functions not merely of the fluid mechanics of pressure and ...
The spinal cord has both vasodilation and vasoconstriction nerves. The neurons that control vascular vasodilation originate in ... These approaches to the mechanism of vasodilation are not mutually exclusive. Vasodilation directly affects the relationship ... Vasodilation is the widening of blood vessels. It results from relaxation of smooth muscle cells within the vessel walls, in ... Vasodilation works to decrease TPR and blood pressure through relaxation of smooth muscle cells in the tunica media layer of ...
ENGLISH: Certain substances (vasodilators; e.g. acetylcholine & prostaglandins) are released to blood in order to regulate the diameter of blood vessels. The...
SEARCH RESULTS for: Arteriolar Vasodilation [Drug Class] (256 results) *Share : JavaScript needed for Sharing tools. Bookmark ...
... 2014-08-27 03:12:30 , BioPortfolio. Home » Topics » Alzheimers Disease » Research » ... Radial Artery Vasodilation Heat Study. The purpose of this study is to collect data about the efficacy of utilizing distal ... More From BioPortfolio on "Topical Radial Artery Vasodilation". *Related Companies*Related Clinical Trials*Related PubMed ...
Evidence for endothelium-dependent vasodilation of resistance vessels by acetylcholine.. Furchgott RF, Carvalho MH, Khan MT, ... In the perfused mesenteric arterial vasculature of the rat, vasodilation by ACh was markedly, though not completely, inhibited ... In the perfused mesenteric arterial vasculature of the rabbit, vasodilation by acetylcholine (ACh) was almost completely ... These results suggest that a major component of vasodilation of mesenteric resistance vessels in rabbit and rat by ACh is ...
A comparison between active- and reactive-hyperaemia-induced brachial artery vasodilation Jaume Padilla, Ryan A. Harris, Alyce ... Insulin increases glycolysis without further vasodilation in porcine coronary arteries exposed to hypoxia Ole FRØBERT, Jens P. ...
Forty-seven papers on the mechanisms whereby natural regulatory phenomena and synthetic vasodilator agents effect vasodilation ... From a symposium, Mechanisms of Vasodilation, held July 1980 in Belgium. Five sections: neurohumoral regulation, local ... Vasodilation.. Ann Intern Med. 1982;96:132. doi: ...
In addition, vasodilation in response to NaHS treatment was decreased in aortic rings from eNOS-/- mice and in those from wild- ... Two Gases Required for Vasodilation and Angiogenesis Message Subject. (Your Name) has forwarded a page to you from Science ... Thus, NO and H2S signaling synergize to promote vasodilation and angiogenesis in endothelial cells by increasing cGMP-dependent ... The gasotransmitters hydrogen sulfide (H2S) and nitric oxide (NO) trigger dilation of blood vessels (called vasodilation) and ...
Endothelium-Independent Vasodilation SNP produced a dose-dependent vasodilation that was similar among the experimental groups ... Effect of Methylene Blue on ACh- and SNP-Induced Vasodilation Methylene blue inhibited both vasodilation induced by ACh and ... IC has significantly less inhibitory effect with SNP vasodilation than with endothelium-dependent vasodilation by ACh, ... IC inhibited the SNP-induced vasodilation to a lesser extent than vasodilation to ACh, histamine, or A23187 (Fig 4B⇓). Whereas ...
... Study Abstract. BACKGROUND: Recent evidence supports differential effects ...
E. Skorupska, M. Rychlik, W. Pawelec, and A. Bednarek, "Intensive short-term vasodilation effect in the pain area of sciatica ... Dry Needling Related Short-Term Vasodilation in Chronic Sciatica under Infrared Thermovision. Elżbieta Skorupska,1 Michał ... K. Kimura, H. Takeuchi, K. Yuri, and I. Wakayama, "Effects of nitric oxide synthase inhibition on cutaneous vasodilation in ...
Vasodilation is one of the most prominent effects of adenosine and one of the first to be recognized, but its mechanism of ... These doses were chosen to produce comparable levels of vasodilation. In a separate study, a second saline infusion was ... Role of nitric oxide in adenosine-induced vasodilation in humans.. Costa F1, Biaggioni I. ... As expected, pretreatment with L-NMMA reduced acetylcholine-induced vasodilation; 50 microg/min acetylcholine increased forearm ...
Tags: arginine, bloos pressure, erectile dysfunction, nitric oxide, NO, soy isoflavones, vasodilation, vasodilators ... There are many reasons people may want to increase nitric oxide production and vasodilation; better blood pressure, improved ... In response, the supplement industry has created a whole category of supplements to promote vasodilation (" nitric oxide ... is a highly desirable natural compound that promotes better circulation by inducing a natural process known as vasodilation. ...
Nitric Oxide-Dependent Vasodilation in Young Spontaneously Hypertensive Rats. Alberto Radaelli, Luca Mircoli, Ileana Mori, ... Preserved endothelium-dependent vasodilation in patients with essential hypertension. N Engl J Med. 1994;330:1036-1040. ... Nitric Oxide-Dependent Vasodilation in Young Spontaneously Hypertensive Rats. Alberto Radaelli, Luca Mircoli, Ileana Mori, ... Nitric Oxide-Dependent Vasodilation in Young Spontaneously Hypertensive Rats. Alberto Radaelli, Luca Mircoli, Ileana Mori, ...
Capillary endothelium Endothelial basement membrane Interstitial space Epithelial basement membrane Alveolar epithelium ( type I pneumocyte) (thick , upper - fluid & gas  On one side of alveolar septum  On the other side exchanging side) there is connective tissue and interstitial space (thin , down- gas exchange only) basement membranes are fused and there is a greatly restricted interstitial space 55 .    There are tight junctions on the epithelium of the upper side (passage of fluid from interstitial space to alveolus) There are loose junction on the endothelium of the upper side (passage of fluid from intravascular space to interstitial space) Pulmonary capillary permeability depends on the size & number of loose junctions 56 . 1. 2. Interstitial space is between periarteriolar and peribronchial connective tissue shit and between epithelium & endothelium basement membrane in alveolar septum The space has a progressively negative distal to proximal ΔP Negative ΔP increases ...
Unveiling the Mechanism of Coronary Metabolic VasodilationVoltage-Gated Potassium Channels and Hydrogen Peroxide Dawid ...
Cannabinoid-induced mesenteric vasodilation through an endothelial site distinct from CB1 or CB2 receptors. Zoltán Járai, Jens ... Anandamide-induced vasodilation (●) is inhibited in the presence 10 μM cannabidiol (○) in rat mesenteric arteries. Points and ... Each panel represents a separate preparation, illustrating the long lasting vasodilation by 4 mg of Abn-cbd (A), and its ... Cannabinoid-induced mesenteric vasodilation through an endothelial site distinct from CB1 or CB2 receptors ...
Vasodilation in Patients With Fabrys Disease. The safety and scientific validity of this study is the responsibility of the ... This process is referred to as vasodilation. It is controlled by a substance released by cells in blood vessels called EDRF ( ... If found to be abnormal, endothelial-derived vasodilation will serve as a useful clinical outcome measure in the evaluation of ... Several drugs can affect vasodilation. Researchers believe some drugs may work by blocking the affect of EDRF. Researchers ...
This process is referred to as vasodilation. It is controlled by a substance released by cells in blood vessels called EDRF ( ... If found to be abnormal, endothelial-derived vasodilation will serve as a useful clinical outcome measure in the evaluation of ... Several drugs can affect vasodilation. Researchers believe some drugs may work by blocking the affect of EDRF. Researchers ... The role of nitric oxide in endothelium-dependent vasodilation of hypercholesterolemic patients. Circulation. 1993 Dec;88(6): ...
Nitroglycerin-induced vasodilation was similar in the 2 groups (10.1±1.4% versus 10.8±0.7% from baseline; P,0.05). In all ... Vasodilation to acetylcholine in primary and secondary forms of human hypertension. Hypertension. 1993; 21: 929-933. ... Effect of treatment on flow-dependent vasodilation of the brachial artery in essential hypertension. Hypertension. 1999; 33: ... vasodilation. Received July 28, 2003; de novo received December 17, 2003; revision received February 19, 2004; accepted ...
To determine whether NE can also elicit peripheral beta 1-adrenergic vasodilation, conscious dogs were studied a ... To determine whether NE can also elicit peripheral beta 1-adrenergic vasodilation, conscious dogs were studied after recovery ... beta 1-Adrenergic blockade with atenolol reversed the vasodilation induced by NE completely, while at this time isoproterenol ... either administration of NE or release of endogenous NE elicits potent peripheral vasodilation, which appears to involve a beta ...
DESIGN: Endothelium-dependent vasodilation and endothelium-independent vasodilation (EIDV) was studied in the forearm during ... 5. The effect of a mixed meal on endothelium-dependent vasodilation is dependent on fat content in healthy humans. Open this ... Impaired endothelium-dependent vasodilation (EDV) is an early marker of atherosclerosis. The aim of the present study was to ... Endothelium-dependent vasodilation (EDV), LDL particle size, and antibodies against oxidized LDL (oxLDLab) have been shown to ...
The Constant Direct Current Electrotherapy Physiotherapy - Free download as PDF File (.pdf), Text File (.txt) or read online for free. CONSTANT DIRECT CURRENT IN ELECTROTHERAPY FOR PHYSIOTHERAPISTS
This study addresses whether cutaneous vasodilation occurs normally in diabetic subjects in response to a standard exercise of ... Defective Vasodilation Response to Exercise in Cutaneous Precapillary Vessels in Diabetic Humans. ... Defective Vasodilation Response to Exercise in Cutaneous Precapillary Vessels in Diabetic Humans ... Defective Vasodilation Response to Exercise in Cutaneous Precapillary Vessels in Diabetic Humans ...
NO initiates and maintains vasodilation through a cascade of biological events that culminate in the relaxation of smooth ... NO initiates and maintains vasodilation through a cascade of biological events that culminate in the relaxation of smooth ... Home / Resources / Featured Writers / Nitric Oxide Series, Part Four: How Nitric Oxide (NO) Causes Vasodilation ... To induce vasodilation, the body must reduce these biologic responses or counter them with vasodilators such as NO (or a ...
Vasodilation was again scored at 1, 2, 3, 4, 5 and 6 hours after dosing. Incidence of vasodilation was calculated as the ... Further clinical studies would be needed to determine whether the higher incidence of vasodilation may also be attributed to ... The objective of this in vivo study was to compare the incidence of vasodilation in guinea pigs following topical ... magnification to score ocular vasodilation (a measure of hyperemia), using a scoring system developed at Alcon Research, Ltd. ...
What is reflex vasodilation? Meaning of reflex vasodilation medical term. What does reflex vasodilation mean? ... Looking for online definition of reflex vasodilation in the Medical Dictionary? reflex vasodilation explanation free. ... reflex vasodilation. reflex vasodilation. Etymology: L, reflectere, to bend back, vas, vessel, dilatare, to spread out ... It occurs secondary to a sudden reflex vasodilation or bradycardia, or both.. Syncope and the runner ...
Addition of TEA to L-NMMA further reduced exercise-induced vasodilation by 9%, p=0.002 in the Healthy, and 18%, p=0.005 in HC ... Results: Exercise-induced vasodilation produced a stepwise increase in FBF in both groups (p,0.0001). At peak (45%) exercise, ... Conclusions: This study demonstrates for the first time that compared to healthy subjects, exercise-induced vasodilation is A) ... We hypothesized that there is a differential contribution of these two agonists to exercise-induced vasodilation. ...
Richmond KN, Tune JD, Gorman MW, Feigl EO: Role of K+ATP channels in local metabolic coronary vasodilation. Am J Physiol Heart ... Duncker DJ, Van Zon NS, Altman JD, Pavek TJ, Bache RJ: Role of K+ATP channels in coronary vasodilation during exercise. ... Most notably, glibenclamide also significantly attenuates adenosine-mediated coronary vasodilation (2,4,5,11,13, 24,25). ... This study is the first to show that KATP channels contribute to local metabolic coronary vasodilation in experimental diabetic ...
Vasoactive intestinal polypeptide-like substance: the potential transmitter for cerebral vasodilation. By TJ Lee, A Saito, I ... Vasoactive intestinal polypeptide-like substance: the potential transmitter for cerebral vasodilation. By TJ Lee, A Saito, I ... These results provide strong evidence in favor of the hypothesis that a VIP-like substance is the transmitter for vasodilation ... Vasoactive intestinal polypeptide-like substance: the potential transmitter for cerebral vasodilation Message Subject. (Your ...
  • These findings indicate that K ATP channels contribute to local metabolic coronary vasodilation in alloxan-induced diabetic dogs. (
  • These studies indicate that K ATP channels are important in regulating coronary vascular resistance under baseline conditions ( 3 - 10 ), during hypoxic coronary vasodilation ( 11 , 12 ), and during reactive coronary hyperemia ( 1 , 4 , 13 ). (
  • 14 ) found that diabetes enhanced K ATP channel-mediated coronary vasodilation of coronary arterioles, suggesting that K ATP channels are important in local metabolic coronary vasodilation in diabetes. (
  • Despite this fact, no study has examined whether K ATP channels contribute to metabolic coronary vasodilation in an intact diabetic model. (
  • Accordingly, this study was designed to determine whether K ATP channels contribute to local metabolic coronary vasodilation in diabetic subjects. (
  • The possibility of bradykinin being a mediator in the coronary vasodilation produced by epinephrine has been discussed. (
  • Our findings suggest that insulin increases arterial glycolysis, but treatment with insulin, propranolol, or both, is not associated with enhanced coronary vasodilation during hypoxia. (
  • Background: Impaired coronary vasodilation to both endothelial-dependent and endothelial-independent stimuli have been associated with atherosclerosis. (
  • Direct measurement of coronary vasodilation using x-ray angiography or intravascular ultrasound is invasive and, thus, not appropriate for asymptomatic patients or for serial follow-up. (
  • Coronary cross sectional area (CSA) was measured on pre-and post-NTG images and % coronary vasodilation was calculated. (
  • Results: Patients with DM and ESRD had impaired coronary vasodilation to NTG compared to age-matched controls (17.8 +/- 7.3% vs. 25.6 +/- 7.1%, p = 0.002). (
  • Conclusion: Noninvasive coronary CMR demonstrates impairment of coronary vasodilation to NTG in high-risk patients with DM and ESRD. (
  • This study tested the hypothesis that obesity diminishes the contribution of K v channels to coronary vasodilation in response to hypoxemia. (
  • These data support that K v channels contribute to increases in coronary flow in response to hypoxemia in lean swine and that reductions in K v channel function contribute to impaired hypoxic coronary vasodilation in obese swine. (
  • Pressure-flow characteristics of coronary stenoses in unsedated dogs at rest and during coronary vasodilation. (
  • The pressure-flow characteristics of 100 left circumflex stenoses in 10 chronically instrumented unsedated dogs were studied under resting conditions and during pharmacological coronary vasodilation. (
  • The injection of Hypaque into the left coronary artery resulted in a forearm vasodilation which could not be duplicated by an injection of a comparable amount of contrast into the ascending aorta, three centimeters above the coronary ostia. (
  • Renografin injected into the left coronary artery resulted in less forearm vasodilation (21% increase in forearm blood flow and 32% decrease in forearm vascular resistance). (
  • When coronary arteriography was repeated following injection of atropine into the brachial artery, no forearm vasodilation occurred. (
  • It is suggested that in human subjects myocardial or coronary artery receptors can be activated by the intracoronary injection of iodinated contrast media which results in a forearm vasodilation. (
  • Vasodilation occurs in the time phase of cardiac systole, whereas vasoconstriction follows in the opposite time phase of cardiac diastole. (
  • One possibility for this discrepancy is that cerebral vasoconstriction during hyperventilation immediately before rebreathing may attenuate cerebral vasodilation and thus, CBF responses during the subsequent hypercapnic rebreathing. (
  • A similar pattern of an initial general vasoconstriction followed by hindquarter vasodilation can be seen after stimulation of S -α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in the NTS ( 9 ). (
  • Cards with brief descriptions of Vasodilation and Vasoconstriction. (
  • A sequence of vasoconstriction followed by vasodilation that acts as a protective mechanism to prevent cold weather injury to the extremities. (
  • How does vasoconstriction/vasodilation change blood pressure? (
  • We apply wavelet-based time-localized phase coherence to investigate the relationship between blood flow and skin temperature, and between blood flow and instantaneous heart rate (IHR), during vasoconstriction and vasodilation provoked by local cooling or heating of the skin. (
  • We conclude that the mechanisms of vasodilation and vasoconstriction, in response to temperature change, are oscillatory in nature and are independent of central sources of variability. (
  • This diagram demonstrates comparative differences within vein structure during states of vasodilation, vasoconstriction, and normality. (
  • In contrast to our findings during brief cold exposure, we showed that cutaneous vasoconstriction during prolonged cold stress is potentiated by hypoxia and abolishes hypoxic vasodilation. (
  • Unless you're bleeding, but if you're bleeding the body will undergo vasoconstriction not vasodilation so the answer is never. (
  • Conclusions- These data demonstrate a strong association between aldosterone excess and impaired endothelial function in human subjects as indexed by flow-mediated arterial vasodilation. (
  • Flow-mediated vasodilation (FMD) is a non-invasive ultrasound method of evaluating endothelial function. (
  • Flow mediated vasodilation and gestational diabetes" by Joseph T. Kowalski, Donna A. Santillan et al. (
  • To prospectively measure flow mediated vasodilation (FMD) in a cohort of women with risk factors for preeclampsia and to identify poor obstetrical outcomes associated with changes in FMD. (
  • Brachial artery measures including flow-mediated vasodilation (FMD), nitroglycerinmediated vasodilation (NMD), brachial artery diameter (BAD), FMD/NMD ratio and post-nitroglycerin brachial artery diameter (P-NTGD) examinations were studied in all subjects by using brachial artery ultrasonography. (
  • Vasodilation works to decrease TPR and blood pressure through relaxation of smooth muscle cells in the tunica media layer of large arteries and smaller arterioles. (
  • Vasodilation is widening of blood vessels caused by relaxation of smooth muscle cells in the vessel walls particularly in the large arteries , smaller arterioles and large veins thus causing an increase in blood flow [ 6 ]. (
  • Superoxide anion radical does not mediate vasodilation of cerebral arterioles by vasoactive intestinal polypeptide. (
  • The term vasodilation refers to the dilation or relaxation of the arterioles to allow more blood to an area. (
  • Endogenous substances and drugs that cause vasodilation are termed vasodilators. (
  • Drugs that cause vasodilation are called vasodilators . (
  • What cause Vasodilation? (
  • There are several medications and innate substances that can cause vasodilation (increase in the diameter of the blood vessels). (
  • Localized tissues have multiple ways to increase blood flow, including releasing vasodilators, primarily adenosine, into the local interstitial fluid, which diffuses to capillary beds, provoking local vasodilation. (
  • Apyrase, an enzyme in tick saliva, may maintain blood flow into the bite by stimulating local vasodilation and preventing platelet aggregation. (
  • 1:57] There, inhaled nitric oxide activates transduction pathways, [2:00] relaxing the smooth muscle cells, [2:07] which results in selective and local vasodilation … Nitric oxide, also called nitrogen oxide or nitrogen monoxide, is produced by almost every cell of the human body. (
  • Local vasodilation was evoked by the application of nitric oxide (NO) donor nitroglycerin into a well, fixed 2 mm above the marginal gingiva, in 20 subjects with healthy periodontal tissue. (
  • Thus, NO and H 2 S signaling synergize to promote vasodilation and angiogenesis in endothelial cells by increasing cGMP-dependent signaling. (
  • In response, the supplement industry has created a whole category of supplements to promote vasodilation (" nitric oxide boosters") most of which rely on, essentially, a single amino acid to get job done. (
  • Nitric oxide is a gas that's made by your body, and one of its primary purposes is to promote vasodilation, or increased blood flow. (
  • We conclude that VIP does not cause generation of superoxide and that superoxide or other reactive oxygen species derived from it, such as hydrogen peroxide and hydroxyl radical, are not mediators of the cerebral vasodilation caused by VIP. (
  • This study addresses whether cutaneous vasodilation occurs normally in diabetic subjects in response to a standard exercise of underlying muscle. (
  • Menthol induces cutaneous vasodilation, however the underlying mechanisms are unknown. (
  • The purpose of this study was to determine the mechanisms contributing to menthol-mediated cutaneous vasodilation and to establish a time course for menthol appearance/clearance in the skin. (
  • Menthol induces cutaneous vasodilation in the skin through multiple vasodilator pathways, including NO, EDHF, and sensory nerves. (
  • We found that hypoxia stimulates cutaneous vasodilation in men whereas skin blood flow is unaltered in women. (
  • In the perfused mesenteric arterial vasculature of the rabbit, vasodilation by acetylcholine (ACh) was almost completely blocked after a 15-min perfusion of the vasculature with 0.2% collagenase, an enzyme capable of removing endothelial cells. (
  • In the perfused mesenteric arterial vasculature of the rat, vasodilation by ACh was markedly, though not completely, inhibited by hemoglobin (10 microM), an agent which can inactivate endothelium-derived relaxing factor (EDRF). (
  • These results suggest that a major component of vasodilation of mesenteric resistance vessels in rabbit and rat by ACh is mediated by EDRF. (
  • Anandamide-induced vasodilation (●) is inhibited in the presence 10 μM cannabidiol (○) in rat mesenteric arteries. (
  • Capsaicine-induced mesenteric vasodilation is competitively inhibited by capsazepine, but not by SR141716A. (
  • Contribution of K+ channels to arachidonic acid-induced endothelium-dependent vasodilation in rat isolated perfused mesenteric arteries. (
  • The contribution of K+ channels and cytochrome P450 generated arachidonic acid (AA) metabolites to the endothelium-dependent vasodilation produced by this fatty acid in the perfused rat isolated mesenteric arteries was examined using a variety of compounds known to inhibit transmembrane K+ channels and cytochrome P450 enzymes. (
  • We have used traditional bioassay techniques to show that ATP-induced vasodilation in mesenteric vessels is endothelium-dependent. (
  • Together, these results show that ATP-induced vasodilation is mediated by P2X1 receptor activation on mesenteric arterial endothelial cells. (
  • Vasodilation caused by relaxation of smooth muscle cells in arteries causes an increase in blood flow. (
  • Impact of local endothelial challenge with cytomegalovirus or glycoprotein B on vasodilation in intact pressurized arteries from nonpregnant and pregnant mice. (
  • This study sought to determine the receptors involved in VIP-induced vasodilation of porcine basilar arteries. (
  • This study shows that all known VIP receptors are involved in VIP-mediated vasodilation of porcine basilar arteries. (
  • 5 min of cuff ischaemia) of the radial and brachial arteries in 33 normal subjects and in 13 patients with Type II diabetes, known to have impaired NO-mediated vasodilation. (
  • Abstract To investigate the potential mechanisms by which indigo carmine produces hypertension, we tested the hypothesis that indigo carmine inhibits endothelium-dependent vasodilation and determined the possible site of the inhibition (endothelium versus smooth muscle). (
  • 19 Inhibition of any site in this l -arginine-NO-guanylyl cyclase pathway can cause an impairment of endothelium-dependent vasodilation and hypertension. (
  • Abstract -Conflicting evidence exists on the possible impairment of tonic nitric oxide (NO)-mediated vasodilation as a causative factor in the genesis of human as well as experimental hypertension. (
  • In conclusion, our observations indicate that during the developmental phase of hypertension in the SHR model, namely, during the prehypertensive as well as the early established hypertensive stage, NO-dependent vasodilation is preserved (if not enhanced) so that a putative impairment of this function provides no significant pathogenic contribution to the onset of hypertension in this experimental model. (
  • Growing attention is being given to endothelial function in hypertension and to the possibility that an inadequate nitric oxide (NO)-mediated vasodilation may be of pathogenic importance in the onset and maintenance of the hemodynamic hallmark of the disease, ie, the elevation in peripheral vascular resistance. (
  • Hemorheologic effects of vasodilation in essential hypertension. (
  • Because hypertension has been associated with endothelial dysfunction, the aim of the study was to compare forearm TPA release and vasodilation in response to muscarinic stimulation in normotensive (NC) and borderline hypertensive (BH) subjects. (
  • Although there are both references relating to the fact that endothelial dysfunction may precede insulin resistance ( 11 , 12 ) and unique recent work concerning the relationship between the spillover markers of endothelial dysfunction and incident diabetes ( 13 ), a clear relationship between endothelium-dependent vasodilation and diabetes has, to our knowledge, never been demonstrated. (
  • Insulin-mediated skeletal muscle vasodilation is nitric oxide dependent. (
  • In summary, insulin-mediated vasodilation is EDNO dependent. (
  • Insulin vasodilation of skeletal muscle vasculature most likely occurs via increasing EDNO synthesis/release. (
  • The present study was designed to investigate whether insulin (1.4×10 −7 M) and the β-adrenoceptor antagonist, propranolol (10 −5 M), increase hypoxic vasodilation in correspondence with changes in glycolysis. (
  • Treatment with insulin quadrupled the lactate/pyruvate ratio during hypoxia, but did not change hypoxic vasodilation. (
  • Insulin stimulates the renin-angiotensin system and induces renal vasodilation. (
  • Insulin-induced activation of the renin-angiotensin system modulates insulin-induced renal vasodilation in healthy individuals. (
  • We sought to examine the relationship between insulin-induced renal vasodilation and insulin-induced activation of the RAS. (
  • We examined the relationships between insulin-induced renal vasodilation, insulin-induced renin secretion, and insulin-induced sensitization of the renal vasculature to ARB. (
  • Evidence for endothelium-dependent vasodilation of resistance vessels by acetylcholine. (
  • Indigo carmine (10 −4 mol/L) also inhibited endothelium-independent vasorelaxation induced by sodium nitroprusside (an activator of vascular smooth muscle soluble guanylyl cyclase), although to a lesser extent than vasodilation from acetylcholine, histamine, and Ca 2+ ionophore A23187. (
  • The goals of the present study were (1) to examine whether IC inhibits endothelium-dependent vasodilation and (2) to determine whether the site of the inhibition is at the endothelium or at the vascular smooth muscle soluble guanylyl cyclase level. (
  • Impaired endothelium-dependent vasodilation (EDV) is associated with atherosclerotic cardiovascular disease as well as several of its risk factors. (
  • Apolipoprotein B was inversely associated with both EDV and endothelium-independent vasodilation (EIDV) in healthy subjects aged 20-69 years. (
  • Endothelium-dependent vasodilation (EDV), LDL particle size, and antibodies against oxidized LDL (oxLDLab) have been shown to be related to the development of atherosclerosis and cardiovascular disease. (
  • However, the relationship of endothelium-dependent vasodilation and diabetes has never been prospectively evaluated. (
  • Abstract We recently showed that muscarinic receptor stimulation causes a marked increase in the net release of tissue-type plasminogen activator (TPA) antigen and activity across the human forearm in vivo, in conjunction with endothelium-dependent vasodilation. (
  • Endothelium-dependent vasodilation and endothelial TPA release in response to muscarinic receptor stimulation were preserved in BH subjects. (
  • AA (1-1000 nmol) caused dose- and endothelium-dependent vasodilation in the presence of indomethacin and the effect was neither altered by lipoxygenase (AA 861) nor cytochrome P450 monooxygenase (alpha-naphthoflavone, ketoconazole and metyrapone) inhibitors indicating that AA-induced, endothelium-dependent vasodilation in this vascular bed was not mediated by product(s) of AA metabolism. (
  • Mild pre-acidification caused by the pH 7.2 Krebs solution enhanced the lipid emulsion-mediated reversal of levobupivacaine-induced vasodilation in isolated endothelium-intact aortic rings, whereas mild pre-acidification caused by the pH 7.2 Krebs solution did not significantly alter the lipid emulsion-mediated reversal of the levobupivacaine-induced vasodilation in isolated endothelium-denuded aortic rings or endothelium-intact aortic rings with L-NAME. (
  • Taken together, these results suggest that mild pre-acidification enhances the lipid emulsion-mediated reversal of toxic dose levobupivacaine-induced vasodilation in the endothelium-intact aorta via the inhibition of nitric oxide. (
  • This study assessed methacholine-stimulated (endothelium-dependent) vasodilation of forearm resistance vessels as a function of age in 119 healthy subjects (19-69 years). (
  • Vasodilation induced by Ro-25-1553, the VPAC2 agonist, was unaffected by NOS inhibition or removal of the endothelium. (
  • Activation of the NPR-C receptor produced a vasodilation, which was susceptible to NOS inhibition and independent of endothelium. (
  • The VPAC1 receptor is located on the endothelium and elicits vasodilation by generating nitric oxide (NO). The VPAC2 receptor is mainly expressed in the outer layers of the smooth muscle and induces vasodilation independently of NO in response to VIP released from intramural nerves. (
  • The NPR-C receptor produces NO-dependent vasodilation independently of the endothelium by stimulation of nNOS in intramural nerves. (
  • TNF-α-induced endothelium-independent vasodilation: a role for phospholipase A2-dependent ceramide signaling. (
  • Peripheral vasodilation is influenced by NO (nitric oxide) released from vascular endothelium in response to increased vessel wall shear stress, and absorption by Hb is the main mechanism by which the bioactivity of NO is disarmed. (
  • Thus, in normal subjects, NO-mediated endothelium-related vasodilation at least partly out-balanced the 'added burden' of a low [Hb] during post-ischaemic reperfusion. (
  • L-arginine improves endothelium-dependent vasodilation in hypercholesterolemic humans. (
  • Endothelium-dependent vasodilation is impaired in hypercholesterolemia, even before the development of atherosclerosis. (
  • The purpose of this study was to determine whether infusion of L-arginine, the precursor of the endothelium-derived relaxing factor, nitric oxide, improves endothelium-dependent vasodilation in hypercholesterolemic humans. (
  • The vasodilative response to the endothelium-dependent vasodilator, methacholine chloride, was depressed in the hypercholesterolemic group, whereas endothelium-independent vasodilation, induced by nitroprusside, was similar in each group. (
  • It is concluded that endothelium-dependent vasodilation is impaired in hypercholesterolemic humans. (
  • It induces endothelium dependent vasodilation, but the precise receptor pathway activated in this response is currently under debate. (
  • The effects of vasodilation, how the blood quantity increases and decreases along with the blood flow and the arterial blood flow and resistance on cardiac output is discussed in this review Article. (
  • It is concluded that, although overall vasodilation occurs normally in diabetic cutaneous circulation, the mechanism is different from the normal response in that flow increases by augmentation of capillary flow rather than by recruitment. (
  • It occurs secondary to a sudden reflex vasodilation or bradycardia, or both. (
  • Systemic arterial vasodilation occurs very early in the first trimester of pregnancy. (
  • 7 In other clinical circumstances of arterial underfilling, whether as a result of a decrease in cardiac output from heart failure or systemic arterial vasodilation as occurs with cirrhosis, increases in the renin-angiotensin-aldosterone system, hypotonicity, and hyponatremia all are common occurrences. (
  • A subsequent vasodilation occurs in the hindquarter bed ( 4 ). (
  • Arteriolar vasodilation occurs. (
  • Although it is recognized that the sympathetic nervous system plays an expendable role in vasodilation, it is only one of the mechanisms by which vasodilation can be accomplished. (
  • Forty-seven papers on the mechanisms whereby natural regulatory phenomena and synthetic vasodilator agents effect vasodilation. (
  • From a symposium, Mechanisms of Vasodilation, held July 1980 in Belgium. (
  • Our results demonstrate, for the first time, that affinin induces vasodilation by mechanisms that involve gasotransmitters, and prostacyclin signaling pathways. (
  • 5 6 7 We recently applied the perfused-forearm model to study the in vivo release mechanisms of TPA in humans 8 9 and found that muscarinic receptor stimulation by MCh, in addition to producing pronounced vasodilation, elicited a marked increase in the net release of TPA antigen and increment of TPA activity across forearm tissues. (
  • A low [Hb] (Hb concentration) is out-balanced by peripheral vasodilation via mechanisms that are incompletely understood. (
  • Vasodilation is the widening of blood vessels. (
  • Vasodilation is the result of relaxation in smooth muscle surrounding the blood vessels. (
  • There are three main intracellular stimuli that can result in the vasodilation of blood vessels. (
  • Vasodilation is where blood vessels widen. (
  • The gasotransmitters hydrogen sulfide (H 2 S) and nitric oxide (NO) trigger dilation of blood vessels (called vasodilation) and angiogenesis, which requires proliferation and migration of endothelial cells. (
  • These results provide strong evidence in favor of the hypothesis that a VIP-like substance is the transmitter for vasodilation in cerebral blood vessels. (
  • Acidosis causes vasodilation in many different blood vessels, including those in the brain and heart. (
  • We identified a need and designed the experiment with the purpose of determining the effectiveness of Nitrosigine® and CM compared to placebo, in up-regulating NO production in blood vessels as measured by acute changes in vasodilation. (
  • Vasodilation can be described as a widening of the veins and blood vessels which results from the relaxation of smooth muscle cells within the vessel walls. (
  • ATP did not induce vasodilation in vessels from P2X -/-1 mice, confirming an absolute requirement for this receptor. (
  • The act of vasodilation is the widening of blood vessels when the walls of blood vessels relax. (
  • 15 16 17 18 NO thus formed in endothelial cells causes vasodilation by stimulating vascular smooth muscle soluble guanylyl cyclase and elevating cGMP levels. (
  • Epoxyeicosatrienoic acids and prostaglandins are unlikely to be primary mediators of flicker light-induced retinal vasodilation in humans. (
  • Retinal vasodilation, a surrogate marker of hyperemia, is a normal physiological response to flicker light stimulation. (
  • Hypoxic vasodilation, interstitial lactate/pyruvate ratio and interstitial glucose were measured at low (2 mM) and high (20 mM) glucose concentrations. (
  • Systemic arterial vasodilation in early pregnancy is accompanied by a compensatory rise in cardiac output and a decline in BP. (
  • therefore, at least early in gestation, arterial vasodilation cannot be explained by arteriovenous shunting through the placenta. (
  • Estrogens are known to upregulate nitric oxide (NO) synthase, 2 and there is experimental evidence that NO contributes to this arterial vasodilation during pregnancy. (
  • 3 , 4 Moreover, an increase in circulating relaxin during early pregnancy is also known to increase NO-mediated arterial vasodilation. (
  • 5 Systemic arterial vasodilation in pregnancy is associated consequently with a secondary increase in cardiac output. (
  • 1 This increase in cardiac output is inadequate, however, to compensate for the arterial vasodilation and diminished systemic vascular resistance. (
  • Compensatory responses, in addition to the increase in cardiac output, occur in association with the arterial vasodilation of pregnancy. (
  • The systemic arterial vasodilation in the first trimester of pregnancy is also associated with stimulation of thirst, increased water intake, and a decline in plasma osmolality of approximately 8 to 10 mOsm/kg H 2 O (4- to 5-mEq/L decline in serum sodium concentration). (
  • A similar nonosmotic stimulation of thirst and release of vasopressin would be expected with the systemic arterial vasodilation of pregnancy. (
  • Furthermore, low-frequency pulsed magnetic therapy activates the parasympathetic nervous system and promotes the efflux of Ca2+ ions, which leads to a relaxation of the blood vessel muscles (especially pre-capillary sphincters) and subsequent vasodilation. (
  • Vasodilation directly affects the relationship between mean arterial pressure, cardiac output, and total peripheral resistance (TPR). (
  • Norepinephrine-induced beta 1-adrenergic peripheral vasodilation in conscious dogs. (
  • To determine whether NE can also elicit peripheral beta 1-adrenergic vasodilation, conscious dogs were studied after recovery from instrumentation for the measurement of cardiac output, arterial pressure, and left ventricular (LV) pressure and calculations of LV dP/dt and total peripheral resistance (TPR). (
  • beta 1-Adrenergic blockade with atenolol reversed the vasodilation induced by NE completely, while at this time isoproterenol was still able to reduce peripheral resistance further, by 67 +/- 7%, indicating that beta 2-adrenergic receptors were not blocked. (
  • Thus, in the presence of alpha-adrenergic receptor blockade, either administration of NE or release of endogenous NE elicits potent peripheral vasodilation, which appears to involve a beta 1-adrenergic receptor mechanism. (
  • The relationship between mean arterial pressure, cardiac output and total peripheral resistance (TPR) gets affected by Vasodilation. (
  • The origin and pathway involved in this neurogenic vasodilation is still unclear ( 4 ), but it was suggested that this vasodilation is caused by peripheral release of preformed nitrosyl factors during sympathetic stimulation ( 6 , 7 ). (
  • Thus we propose that graded NO absorption is the mechanism through which a low [Hb] is related to peripheral vasodilation. (
  • What is peripheral vasodilation? (
  • Vasodilation - The goal of vasodilator therapy are To bring. (
  • Transfection of CSE shRNA in aortic ring explants reduced vasodilation (an effect that was rescued by exogenous application of cGMP) and attenuated increases in cGMP concentrations or phosphorylation of the PKG substrate VASP in response to acetylcholine, DEA/NO, or VEGF. (
  • In addition, the effects of methylene blue on the acetylcholine- and sodium nitroprusside-induced vasodilation were compared with those of indigo carmine. (
  • The inhibition was also greater in the acetylcholine- than the sodium nitroprusside-induced vasodilation. (
  • Role of nitric oxide in adenosine-induced vasodilation in humans. (
  • To investigate the role of epoxyeicosatrienoic acids (EETs) and prostaglandins (PGs) in retinal blood vessel calibers and vasodilation during flicker light stimulation in humans. (
  • We evaluated the tonic NO-dependent vasodilation from the pressor response to NO synthesis inhibition by N G -monomethyl- l -arginine (L-NMMA) in 9 conscious, chronically instrumented spontaneously hypertensive rats (SHR) at 12 weeks of age, ie, during the early established hypertensive stage. (
  • Lipid emulsions, including SMOFlipid ® , Intralipid ® and Lipofundin ® MCT/LCT, reverse severe vasodilation caused by the inhibition of voltage-operated calcium channels induced by toxic doses of levobupivacaine and bupivacaine [ 3 - 5 ]. (
  • In the present study, we demonstrated that the dichloromethane and ethanolic extracts of H. longipes roots, and affinin, isolated from these roots, produce a concentration-dependent vasodilation of rat aorta. (
  • This study provided the opportunity to prospectively assess the association between endothelial vasodilation function, evaluated by ultrasound study of the brachial artery, and the incidence of diabetes among apparently healthy initially nondiabetic postmenopausal women. (
  • Stimulation of a beta receptor causes muscle vasodilation, bronchial relaxation, and cardiac acceleration. (
  • Neither drug affected vasodilation during flicker stimulation. (
  • The primary function of vasodilation is to increase blood flow in the body to tissues that need it most. (
  • In microalbuminuric patients, forearm postischemic vasodilation was also significantly lower and mean awake diastolic blood pressure (dBP) was significantly higher than in the other two groups. (
  • Nitrosigine® is scientifically engineered to boost nitric oxide levels, which have been shown to be a key factor in generating greater blood flow and vasodilation in working muscles. (
  • Citrulline peptide can significantly increase vasodilation and the volume of blood flow compared to raw citrulline and placebo. (
  • Citrulline peptide may be a preferred choice over raw citrulline for athletes seeking enhanced vasodilation or blood flow. (
  • Vasodilation is often accompanied by other coinciding effects such as decreased blood pressure . (
  • Characteristics of the Vasodilation - improved blood circulation program: The low-frequency pulsed magnetic field of Biomag devices improves blood circulation via modification of the polarisation of red blood cells by inducing a positive charge. (
  • To determine if endogenous (ENDG) vasodilation was maximum during myocardial ischemia, left anterior descending (LAD) mean pressure (P) was reduced for 20 min in 13 swine. (
  • Animals were hand-held under 2.75 × magnification to score ocular vasodilation (a measure of hyperemia), using a scoring system developed at Alcon Research, Ltd. Following baseline ocular scoring, each animal received a 30 μL dose to the left eye of either bimatoprost 0.01% (3 μg) or bimatoprost 0.03% (9 μg). (
  • Thus endogenous vasodilation reserve was not used fully during ischemia. (
  • Pulmonary vasodilation in acute pulmonary embolism - a systematic review. (
  • The clinical study poster entitled "The Acute Effects of Citrulline Malate and Bonded Arginine Silicate Supplementation on Vasodilation of Young Adults" was presented by lead author Jeffrey Rogers from the University of Arkansas American College of Sports Medicine. (
  • Entitled "The Acute Effects of Citrulline Malate and Bonded Arginine Silicate Supplementation on Vasodilation of Young Adults," results were presented by lead author Jeffrey Rogers. (
  • In seeming contradiction, acute hyperinsulinemia also induces nitric oxide (NO)-dependent renal vasodilation ( 12 ). (
  • Hypoxia (60 min) caused vasodilation and doubled the lactate/pyruvate ratio. (
  • Vasodilation is one of the most prominent effects of adenosine and one of the first to be recognized, but its mechanism of action is not completely understood. (
  • On the basis of our observations, we conclude that adenosine-induced vasodilation is not mediated by nitric oxide in the human forearm. (
  • Nutrition 21 was excited to hear of this independent study and the positive results showing the benefits of Nitrosigine® on increasing vasodilation, a process driven by increasing nitric oxide production, and believed to enhance a number of sports performance endpoints. (
  • Dephosphorylation by myosin light-chain phosphatase and induction of calcium symporters and antiporters that pump calcium ions out of the intracellular compartment both contribute to smooth muscle cell relaxation and therefore vasodilation. (
  • The vasodilation produced by microinjection of glutamate in the NTS can be reduced by systemic administration of prazosin and N G -nitro- l -arginine methyl ester ( l -NAME) ( 4 ). (
  • This study provided the opportunity to assess the association between endothelial vasodilation function and the incidence of diabetes in a cohort of apparently healthy postmenopausal women. (
  • Many patients with diabetes, however, have no change in palpable temperature due to distal vasodilation related to autonomic neuropathy. (
  • Propranolol blocked isoprenaline-evoked vasodilation, but hypoxic increases in lactate/pyruvate ratio and vasodilation did not change. (