The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
Drugs used to cause constriction of the blood vessels.
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.
The flow of BLOOD through or around an organ or region of the body.
The circulation of the BLOOD through the LUNGS.
Relatively complete absence of oxygen in one or more tissues.
The smallest divisions of the arteries located between the muscular arteries and the capillaries.
The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs.
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
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)
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.
Involuntary contraction or twitching of the muscles. It is a physiologic method of heat production in man and other mammals.
Part of the arm in humans and primates extending from the ELBOW to the WRIST.
The TEMPERATURE at the outer surface of the body.
The circulation of the BLOOD through the vessels of the KIDNEY.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
Arteries which arise from the abdominal aorta and distribute to most of the intestines.
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 processes of heating and cooling that an organism uses to control its temperature.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
The nonstriated involuntary muscle tissue of blood vessels.
Cell surface proteins that bind ENDOTHELINS with high affinity and trigger intracellular changes which influence the behavior of cells.
Compounds that bind to and activate ADRENERGIC ALPHA-1 RECEPTORS.
Drugs that selectively bind to and activate alpha adrenergic receptors.
Drugs used to cause dilation of the blood vessels.
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.
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.
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.
Treatment process involving the injection of fluid into an organ or tissue.
A subtype of endothelin receptor found predominantly in the VASCULAR SMOOTH MUSCLE. It has a high affinity for ENDOTHELIN-1 and ENDOTHELIN-2.
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.
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)
The vessels carrying blood away from the heart.
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 relationship between the dose of an administered drug and the response of the organism to the drug.
A subtype of endothelin receptor found predominantly in the KIDNEY. It may play a role in reducing systemic ENDOTHELIN levels.
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 non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
One of the two major pharmacological subdivisions of adrenergic receptors that were originally defined by the relative potencies of various adrenergic compounds. The alpha receptors were initially described as excitatory receptors that post-junctionally stimulate SMOOTH MUSCLE contraction. However, further analysis has revealed a more complex picture involving several alpha receptor subtypes and their involvement in feedback regulation.
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.
Conditions in which the primary symptom is HEADACHE and the headache cannot be attributed to any known causes.
An alpha-1 adrenergic agonist that causes prolonged peripheral VASOCONSTRICTION.
The veins and arteries of the HEART.
An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems.
The circulation of blood through the BLOOD VESSELS supplying the abdominal VISCERA.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
Venoms from SNAKES of the viperid family. They tend to be less toxic than elapid or hydrophid venoms and act mainly on the vascular system, interfering with coagulation and capillary membrane integrity and are highly cytotoxic. They contain large amounts of several enzymes, other factors, and some toxins.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis.
Peptides whose amino and carboxy ends are linked together with a peptide bond forming a circular chain. Some of them are ANTI-INFECTIVE AGENTS. Some of them are biosynthesized non-ribosomally (PEPTIDE BIOSYNTHESIS, NON-RIBOSOMAL).
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.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
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.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
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.
A subclass of alpha-adrenergic receptors that mediate contraction of SMOOTH MUSCLE in a variety of tissues such as ARTERIOLES; VEINS; and the UTERUS. They are usually found on postsynaptic membranes and signal through GQ-G11 G-PROTEINS.
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 strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
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 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.
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.
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).
Cell surface proteins that bind THROMBOXANES with high affinity and trigger intracellular changes influencing the behavior of cells. Some thromboxane receptors act via the inositol phosphate and diacylglycerol second messenger systems.
An unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).
Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).
A subclass of alpha-adrenergic receptors found on both presynaptic and postsynaptic membranes where they signal through Gi-Go G-PROTEINS. While postsynaptic alpha-2 receptors play a traditional role in mediating the effects of ADRENERGIC AGONISTS, the subset of alpha-2 receptors found on presynaptic membranes signal the feedback inhibition of NEUROTRANSMITTER release.
Recording of change in the size of a part as modified by the circulation in it.
A value equal to the total volume flow divided by the cross-sectional area of the vascular bed.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
Seven membered heterocyclic rings containing a NITROGEN atom.
A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters.
External decompression applied to the lower body. It is used to study orthostatic intolerance and the effects of gravitation and acceleration, to produce simulated hemorrhage in physiologic research, to assess cardiovascular function, and to reduce abdominal stress during childbirth.
An absence of warmth or heat or a temperature notably below an accustomed norm.
A group of intracellular-signaling serine threonine kinases that bind to RHO GTP-BINDING PROTEINS. They were originally found to mediate the effects of rhoA GTP-BINDING PROTEIN on the formation of STRESS FIBERS and FOCAL ADHESIONS. Rho-associated kinases have specificity for a variety of substrates including MYOSIN-LIGHT-CHAIN PHOSPHATASE and LIM KINASES.
Cell surface proteins that bind neuropeptide Y with high affinity and trigger intracellular changes which influence the behavior of cells.
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.
Delivery of drugs into an artery.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
Substances that are used in place of blood, for example, as an alternative to BLOOD TRANSFUSIONS after blood loss to restore BLOOD VOLUME and oxygen-carrying capacity to the blood circulation, or to perfuse isolated organs.
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 circulation of blood through the CORONARY VESSELS of the HEART.
The recording of muscular movements. The apparatus is called a myograph, the record or tracing, a myogram. (From Stedman, 25th ed)
The arterial blood vessels supplying the CEREBRUM.
A competitive inhibitor of nitric oxide synthetase.
Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase.
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.
A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.
Use of electric potential or currents to elicit biological responses.
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.
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 alpha-adrenergic antagonist with long duration of action. It has been used to treat hypertension and as a peripheral vasodilator.
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)
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.
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.
A 36-amino acid peptide present in many organs and in many sympathetic noradrenergic neurons. It has vasoconstrictor and natriuretic activity and regulates local blood flow, glandular secretion, and smooth muscle activity. The peptide also stimulates feeding and drinking behavior and influences secretion of pituitary hormones.
A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures.
Compounds that bind to and activate ADRENERGIC ALPHA-2 RECEPTORS.
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.
A plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of ERECTILE DYSFUNCTION.
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 measure of the level of heat of a human or animal.
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.
A class of drugs that act by selective inhibition of calcium influx through cellular membranes.
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.
Constriction of arteries in the SKULL due to sudden, sharp, and often persistent smooth muscle contraction in blood vessels. Intracranial vasospasm results in reduced vessel lumen caliber, restricted blood flow to the brain, and BRAIN ISCHEMIA that may lead to hypoxic-ischemic brain injury (HYPOXIA-ISCHEMIA, BRAIN).
Drugs that bind to and block the activation of ADRENERGIC ALPHA-1 RECEPTORS.
Antidiuretic hormones released by the NEUROHYPOPHYSIS of all vertebrates (structure varies with species) to regulate water balance and OSMOLARITY. In general, vasopressin is a nonapeptide consisting of a six-amino-acid ring with a cysteine 1 to cysteine 6 disulfide bridge or an octapeptide containing a CYSTINE. All mammals have arginine vasopressin except the pig with a lysine at position 8. Vasopressin, a vasoconstrictor, acts on the KIDNEY COLLECTING DUCTS to increase water reabsorption, increase blood volume and blood pressure.
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)
A stable, non-explosive inhalation anesthetic, relatively free from significant side effects.
A selective serotonin receptor antagonist with weak adrenergic receptor blocking properties. The drug is effective in lowering blood pressure in essential hypertension. It also inhibits platelet aggregation. It is well tolerated and is particularly effective in older patients.
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 potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.
A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).
A serotonin agonist that acts selectively at 5HT1 receptors. It is used in the treatment of MIGRAINE DISORDERS.
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.
Teleost hormones. A family of small peptides isolated from urophyses of bony fishes. They have many different physiological effects, including long-lasting hypotensive activity and have been proposed as antihypertensives. There are at least four different compounds: urotensin I, urotensin II, urotensin III, and urotensin IV.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
The main artery of the thigh, a continuation of the external iliac artery.
A stable, physiologically active compound formed in vivo from the prostaglandin endoperoxides. It is important in the platelet-release reaction (release of ADP and serotonin).
A subclass of eicosanoid receptors that have specificity for THROMBOXANE A2 and PROSTAGLANDIN H2.
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
The movement of the BLOOD as it is pumped through the CARDIOVASCULAR SYSTEM.
Organic compounds containing the -CO-NH2 radical. Amides are derived from acids by replacement of -OH by -NH2 or from ammonia by the replacement of H by an acyl group. (From Grant & Hackh's Chemical Dictionary, 5th ed)
A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.
Non-striated, elongated, spindle-shaped cells found lining the digestive tract, uterus, and blood vessels. They are derived from specialized myoblasts (MYOBLASTS, SMOOTH MUSCLE).
An ergot derivative that is a congener of LYSERGIC ACID DIETHYLAMIDE. It antagonizes the effects of serotonin in blood vessels and gastrointestinal smooth muscle, but has few of the properties of other ergot alkaloids. Methysergide is used prophylactically in migraine and other vascular headaches and to antagonize serotonin in the carcinoid syndrome.
Elements of limited time intervals, contributing to particular results or situations.
The pressure that would be exerted by one component of a mixture of gases if it were present alone in a container. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
A serotonin receptor antagonist in the CENTRAL NERVOUS SYSTEM used as an antipsychotic.
A 21-amino acid peptide that circulates in the plasma, but its source is not known. Endothelin-3 has been found in high concentrations in the brain and may regulate important functions in neurons and astrocytes, such as proliferation and development. It also is found throughout the gastrointestinal tract and in the lung and kidney. (N Eng J Med 1995;333(6):356-63)
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.
The circulation of blood through the BLOOD VESSELS of the BRAIN.
Measurement of oxygen and carbon dioxide in the blood.
Anesthesia caused by the breathing of anesthetic gases or vapors or by insufflating anesthetic gases or vapors into the respiratory tract.
A purinergic P2X neurotransmitter receptor found at sympathetically innervated SMOOTH MUSCLE. It may play a functional role regulating the juxtoglomerular apparatus of the KIDNEY.
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)
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.
A imidazole derivative that is an agonist of ADRENERGIC ALPHA-2 RECEPTORS. It is closely-related to MEDETOMIDINE, which is the racemic form of this compound.
A family of hexahydropyridines.
The removal or interruption of some part of the sympathetic nervous system for therapeutic or research purposes.
An imidazoline sympatholytic agent that stimulates ALPHA-2 ADRENERGIC RECEPTORS and central IMIDAZOLINE RECEPTORS. It is commonly used in the management of HYPERTENSION.
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.
Eicosatetraenoic acids substituted in any position by one or more hydroxy groups. They are important intermediates in a series of biosynthetic processes leading from arachidonic acid to a number of biologically active compounds such as prostaglandins, thromboxanes, and leukotrienes.
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.
A serotonin receptor subtype that is localized to the CAUDATE NUCLEUS; PUTAMEN; the NUCLEUS ACCUMBENS; the HIPPOCAMPUS, and the RAPHE NUCLEI. It plays a role as a terminal autoreceptor that regulates the rate of SEROTONIN release from nerve endings. This serotonin receptor subtype is closely related to and has similar drug binding properties as the 5-HT1B RECEPTOR, but is expressed at low levels. It is particularly sensitive to the agonist SUMATRIPTAN and may be involved in mediating the drug's antimigrane effect.
Drugs that bind to but do not activate serotonin receptors, thereby blocking the actions of serotonin or SEROTONIN RECEPTOR AGONISTS.
The vessels carrying blood away from the capillary beds.
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.
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.
Peptides composed of between two and twelve amino acids.
The main trunk of the systemic arteries.
The blood pressure in the ARTERIES. It is commonly measured with a SPHYGMOMANOMETER on the upper arm which represents the arterial pressure in the BRACHIAL ARTERY.
A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals.
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.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
Benzopyrroles with the nitrogen at the number one carbon adjacent to the benzyl portion, in contrast to ISOINDOLES which have the nitrogen away from the six-membered ring.
Four or five slender jointed digits in humans and primates, attached to each HAND.
Clinical manifestation consisting of a deficiency of carbon dioxide in arterial blood.
The predominant form of mammalian antidiuretic hormone. It is a nonapeptide containing an ARGININE at residue 8 and two disulfide-linked cysteines at residues of 1 and 6. Arg-vasopressin is used to treat DIABETES INSIPIDUS or to improve vasomotor tone and BLOOD PRESSURE.
A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.
The part of the face that is below the eye and to the side of the nose and mouth.
An enzyme found predominantly in platelet microsomes. It catalyzes the conversion of PGG(2) and PGH(2) (prostaglandin endoperoxides) to thromboxane A2. EC
The largest branch of the celiac trunk with distribution to the spleen, pancreas, stomach and greater omentum.
A respiratory stimulant that enhances respiration by acting as an agonist of peripheral chemoreceptors located on the carotid bodies. The drug increases arterial oxygen tension while decreasing arterial carbon dioxide tension in patients with chronic obstructive pulmonary disease. It may also prove useful in the treatment of nocturnal oxygen desaturation without impairing the quality of sleep.
A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of CALCIUM ion on membrane functions.
Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the ADRENERGIC ANTAGONISTS and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals (see ADRENERGIC AGENTS). Drugs that act in the central nervous system to reduce sympathetic activity (e.g., centrally acting alpha-2 adrenergic agonists, see ADRENERGIC ALPHA-AGONISTS) are included here.
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).
Compounds that inhibit the action of prostaglandins.
A serotonin antagonist and a histamine H1 blocker used as antipruritic, appetite stimulant, antiallergic, and for the post-gastrectomy dumping syndrome, etc.
Synthetic compounds that are analogs of the naturally occurring prostaglandin endoperoxides and that mimic their pharmacologic and physiologic activities. They are usually more stable than the naturally occurring compounds.
A subclass of purinergic P2 receptors that signal by means of a ligand-gated ion channel. They are comprised of three P2X subunits which can be identical (homotrimeric form) or dissimilar (heterotrimeric form).
A significant drop in BLOOD PRESSURE after assuming a standing position. Orthostatic hypotension is a finding, and defined as a 20-mm Hg decrease in systolic pressure or a 10-mm Hg decrease in diastolic pressure 3 minutes after the person has risen from supine to standing. Symptoms generally include DIZZINESS, blurred vision, and SYNCOPE.
Nerve fibers liberating catecholamines at a synapse after an impulse.
Cell-surface proteins that bind epinephrine and/or norepinephrine with high affinity and trigger intracellular changes. The two major classes of adrenergic receptors, alpha and beta, were originally discriminated based on their cellular actions but now are distinguished by their relative affinity for characteristic synthetic ligands. Adrenergic receptors may also be classified according to the subtypes of G-proteins with which they bind; this scheme does not respect the alpha-beta distinction.
Sense of awareness of self and of the environment.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
A vasoconstrictor found in ergot of Central Europe. It is a serotonin agonist that has been used as an oxytocic agent and in the treatment of MIGRAINE DISORDERS.
A large vessel supplying the whole length of the small intestine except the superior part of the duodenum. It also supplies the cecum and the ascending part of the colon and about half the transverse part of the colon. It arises from the anterior surface of the aorta below the celiac artery at the level of the first lumbar vertebra.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
Volume of circulating BLOOD. It is the sum of the PLASMA VOLUME and ERYTHROCYTE VOLUME.
Spasm of the large- or medium-sized coronary arteries.
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.
Decarboxylated monoamine derivatives of TRYPTOPHAN.
A 20-carbon unsaturated fatty acid containing 4 alkyne bonds. It inhibits the enzymatic conversion of arachidonic acid to prostaglandins E(2) and F(2a).
The inferior part of the lower extremity between the KNEE and the ANKLE.
Cell-surface proteins that bind SEROTONIN and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action.
The physiologically active and stable hydrolysis product of EPOPROSTENOL. Found in nearly all mammalian tissue.

NaCl-induced renal vasoconstriction in salt-sensitive African Americans: antipressor and hemodynamic effects of potassium bicarbonate. (1/5901)

In 16 African Americans (blacks, 14 men, 2 women) with average admission mean arterial pressure (MAP, mm Hg) 99.9+/-3.5 (mean+/-SEM), we investigated whether NaCl-induced renal vasoconstriction attends salt sensitivity and, if so, whether supplemental KHCO3 ameliorates both conditions. Throughout a 3-week period under controlled metabolic conditions, all subjects ate diets containing 15 mmol NaCl and 30 mmol potassium (K+) (per 70 kg body wt [BW] per day). Throughout weeks 2 and 3, NaCl was loaded to 250 mmol/d; throughout week 3, dietary K+ was supplemented to 170 mmol/d (KHCO3). On the last day of each study week, we measured renal blood flow (RBF) and glomerular filtration rate (GFR) using renal clearances of PAH and inulin. Ten subjects were salt sensitive (SS) (DeltaMAP >+5%) and 6 salt resistant (SR). In NaCl-loaded SS but not SR subjects, RBF (mL/min/1.73 m2) decreased from 920+/-75 to 828+/-46 (P<0.05); filtration fraction (FF, %) increased from 19. 4+/- to 21.4 (P<0.001); and renal vascular resistance (RVR) (10(3)xmm Hg/[mL/min]) increased from 101+/-8 to 131+/-10 (P<0.001). In all subjects combined, DeltaMAP varied inversely with DeltaRBF (r =-0.57, P=0.02) and directly with DeltaRVR (r = 0.65, P=0.006) and DeltaFF (r = 0.59, P=0.03), but not with MAP before NaCl loading. When supplemental KHCO3 abolished the pressor effect of NaCl in SS subjects, RBF was unaffected but GFR and FF decreased. The results show that in marginally K+-deficient blacks (1) NaCl-induced renal vasoconstrictive dysfunction attends salt sensitivity; (2) the dysfunction varies in extent directly with the NaCl-induced increase in blood pressure (BP); and (3) is complexly affected by supplemented KHCO3, GFR and FF decreasing but RBF not changing. In blacks, NaCl-induced renal vasoconstriction may be a pathogenetic event in salt sensitivity.  (+info)

Nitric oxide in the endometrium. (2/5901)

Nitric oxide (NO) is an important mediator of paracrine interactions, especially within the vascular system. It is a powerful inhibitor of platelet aggregation and a potent vasodilator. NO is also a neurotransmitter and it plays a role in cell-mediated cytotoxicity. NO-generating enzymes (nitric oxide synthases, NOS) have been described in the endometrium of a number of species, suggesting that NO might be involved in endometrial function. In human endometrium, endothelial NOS and inducible NOS have been localized to glandular epithelium in the non-pregnant uterus. Weak inducible NOS immunoreactivity has been observed in decidualized stromal cells. NO might participate in the initiation and control of menstrual bleeding. Furthermore, it may play a part in the inhibition of platelet aggregation within the endometrium, where menstrual haemostasis is thought to occur primarily by vasoconstriction rather than clot organization. Endometrially derived NO could also suppress myometrial contractility. Recent attention has focused on the part that NO might play in maintaining myometrial quiescence during pregnancy. NO also appears to relax the non-pregnant myometrium, an action which could be exploited for the medical treatment of primary dysmenorrhoea.  (+info)

Relaxation of endothelin-1-induced pulmonary arterial constriction by niflumic acid and NPPB: mechanism(s) independent of chloride channel block. (3/5901)

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)

O-raffinose cross-linking markedly reduces systemic and renal vasoconstrictor effects of unmodified human hemoglobin. (4/5901)

The hemodynamic effects of a 20% exchange-transfusion with different solutions of highly purified human hemoglobin A-zero (A0) were evaluated. We compared unmodified hemoglobin with hemoglobin cross-linked with O-raffinose. Unmodified hemoglobin increased systemic vascular resistance and mean arterial pressure more than the O-raffinose cross-linked hemoglobin solution (by approximately 45% and approximately 14%, respectively). Unmodified hemoglobin markedly reduced cardiac output (CO) by approximately 21%, whereas CO was unaffected by the O-raffinose cross-linked hemoglobin solution. Unmodified and O-raffinose cross-linked hemoglobin solutions increased mean arterial pressure to comparable extents ( approximately 14% and approximately 9%, respectively). Unmodified hemoglobin increased renal vascular resistance 2-fold and reduced the glomerular filtration rate by 58%. In marked contrast, the O-raffinose cross-linked hemoglobin had no deleterious effect on the glomerular filtration rate, renal blood flow, or renal vascular resistance. The extents to which unmodified and O-raffinose cross-linked hemoglobin solutions inactivated nitric oxide also were compared using three separate in vitro assays: platelet nitric oxide release, nitric oxide-stimulated platelet cGMP production, and endothelium-derived relaxing factor-mediated inhibition of platelet aggregation. Unmodified hemoglobin inactivated or oxidized nitric oxide to a greater extent than the O-raffinose cross-linked hemoglobin solutions in all three assays. In summary, O-raffinose cross-linking substantially reduced the systemic vasoconstriction and the decrease in CO induced by unmodified hemoglobin and eliminated the deleterious effects of unmodified hemoglobin on renal hemodynamics and function. We hypothesize that O-raffinose cross-linking reduces the degree of oxidation of nitric oxide and that this contributes to the reduced vasoactivity of this modified hemoglobin.  (+info)

Protective effect of dietary tomato against endothelial dysfunction in hypercholesterolemic mice. (5/5901)

The effects of dietary ingestion of tomato were studied in mice that had been made hypercholesterolemic by feeding atherogenic diets. Mice which had been fed on the atherogenic diet without tomato for 4 months had significantly increased plasma lipid peroxide, and the vaso-relaxing activity in the aorta induced by acetylcholine (ACh) was harmed when compared with mice fed on a common commercial diet. On the other hand, mice which had been fed on the atherogenic diet containing 20% (w/w) lyophilized powder of tomato showed less increase in the plasma lipid peroxide level, and ACh-induced vaso-relaxation was maintained at the same level as that in normal mice. These results indicate that tomato has a preventive effect on atherosclerosis by protecting plasma lipids from oxidation.  (+info)

Blockade and reversal of endothelin-induced constriction in pial arteries from human brain. (6/5901)

BACKGROUND AND PURPOSE: Substantial evidence now implicates endothelin (ET) in the pathophysiology of cerebrovascular disorders such as the delayed vasospasm associated with subarachnoid hemorrhage and ischemic stroke. We investigated the ET receptor subtypes mediating vasoconstriction in human pial arteries. METHODS: ET receptors on human pial and intracerebral arteries were visualized with the use of autoradiography, and the subtypes mediating vasoconstriction were identified by means of wire myography. RESULTS: ET-1 was more potent than ET-3 as a vasoconstrictor, indicating an ETA-mediated effect. Similarly, the selective ETB agonist sarafotoxin S6c had no effect on contractile action at concentrations up to 30 nmol/L. The nonpeptide ETA receptor antagonist PD156707 (3 to 30 nmol/L) caused a parallel rightward shift of the ET-1-induced response, yielding a pA2 of 9.2. Consistent with these results, PD156707 (30 nmol/L) fully reversed an established constriction in pial arteries induced by 1 nmol/L ET-1, while the selective ETB receptor antagonist BQ788 (1 micromol/L) had little effect. The calcium channel blocker nimodipine (0.3 to 3 micromol/L) significantly attenuated the maximum response to ET-1 in a concentration-dependent manner without changing potency. In agreement with the functional data, specific binding of [125I]PD151242 to ETA receptors was localized to the smooth muscle layer of pial and intracerebral blood vessels. In contrast, little or no [125I]BQ3020 binding to ETB receptors was detected. CONCLUSIONS: These data indicate an important role for ETA receptors in ET-1-induced constriction of human pial arteries and suggest that ETA receptor antagonists may provide additional dilatory benefit in cerebrovascular disorders associated with raised ET levels.  (+info)

Cerebrovascular alterations in protein kinase C-mediated constriction in stroke-prone rats. (7/5901)

BACKGROUND AND PURPOSE: Cerebrovascular pressure-dependent constriction may involve the smooth muscle production of diacylglycerol, which could facilitate constriction by activating protein kinase C (PKC). A dysfunctional PKC system could promote the loss of pressure-dependent constriction. We attempted to determine whether the alterations in pressure-dependent constriction in the middle cerebral arteries (MCAs) observed in relation to stroke development in Wistar-Kyoto stroke-prone spontaneously hypertensive rats (SHRsp) were associated with defects in the ability of the arteries to constrict in response to PKC activation. METHODS: MCAs were sampled from SHRsp before and after stroke development and in stroke-resistant Wistar-Kyoto spontaneously hypertensive rats. A pressure myograph was used to test the ability of the arteries to constrict in response to a 100 mm Hg pressure step and subsequently to contract in response to phorbol 12,13-dibutyrate in the presence of nifedipine (3 micromol/L). RESULTS: Pressure-dependent constriction and constriction in response to phorbol dibutyrate in the MCAs were inhibited by PKC inhibitors (staurosporine [40 nmol/L], chelerythrine [12 micromol/L], bisindolylmaleimide [5 micromol/L]), declined with age before stroke development in SHRsp, and were absent after stroke. There was a significant relationship between pressure- and phorbol dibutyrate-induced constriction (r=0.815, P<0. 05). CONCLUSIONS: Phorbol esters interact with the same activation site as diacylglycerol to stimulate PKC. An inability to constrict in response to phorbol dibutyrate may reflect unresponsiveness to diacylglycerol and may contribute to the loss of pressure-dependent constriction associated with stroke in the MCAs of SHRsp. The loss of this autoregulatory function before stroke could increase the risk of cerebral hemorrhage.  (+info)

Spread of vasodilatation and vasoconstriction along feed arteries and arterioles of hamster skeletal muscle. (8/5901)

1. In arterioles of the hamster cheek pouch, vasodilatation and vasoconstriction can spread via the conduction of electrical signals through gap junctions between cells that comprise the vessel wall. However, conduction in resistance networks supplying other tissues has received relatively little attention. In anaesthetized hamsters, we have investigated the spread of dilatation and constriction along feed arteries and arterioles of the retractor muscle, which is contiguous with the cheek pouch. 2. When released from a micropipette, acetylcholine (ACh) triggered vasodilatation that spread rapidly along feed arteries external to the muscle and arterioles within the muscle. Responses were independent of changes in wall shear rate, perivascular nerve activity, or release of nitric oxide, indicating cell-to-cell conduction. 3. Vasodilatation conducted without decrement along unbranched feed arteries, yet decayed markedly in arteriolar networks. Thus, branching of the conduction pathway dissipated the vasodilatation. 4. Noradrenaline (NA) or a depolarizing KCl stimulus evoked constriction of arterioles and feed arteries of the retractor muscle that was constrained to the vicinity of the micropipette. This behaviour contrasts sharply with the conduction of vasodilatation in these microvessels and with the conduction of vasoconstriction elicited by NA and KCl in cheek pouch arterioles. 5. Focal electrical stimulation produced constriction that spread rapidly along feed arteries and arterioles. These responses were inhibited by tetrodotoxin or prazosin, confirming the release of NA along perivascular sympathetic nerves, which are absent from arterioles studied in the cheek pouch. Thus, sympathetic nerve activity co-ordinated the contraction of smooth muscle cells as effectively as the conduction of vasodilatation co-ordinated their relaxation. 6. In the light of previous findings in the cheek pouch, the properties of vasoconstriction and vasodilatation in feed arteries and arterioles of the retractor muscle indicate that substantive differences can exist in the nature of signal transmission along microvessels of tissues that differ in structure and function.  (+info)

Sleep apnea (SA) affects as many as 20% of the adult population in the United States. It elicits intermittent hypoxia (IH) and causes pulmonary hypertension (PH), however the mechanisms of this PH have not been well studied. IH has been shown to cause polycythemia, pulmonary vascular remodeling and increases in vasoconstrictor reactivity. CO2 supplementation may be protective in the development of PH, therefore we assessed effects of IH with and without CO2 supplementation on indices of PH and pulmonary vasoconstrictor reactivity. IH with CO2 supplementation resulted in eucapnic IH (E-IH) and the lack of polycythemia or vascular remodeling. However, E-IH caused significant right ventricular hypertrophy and increased pulmonary vasoconstrictor reactivity, which was mediated by vascular smooth muscle (VSM) Ca2+ sensitization. We, therefore, sought to determine the mechanism of this enhanced vasoconstrictor reactivity by assessing vasoconstriction and VSM Ca2+ responses to the endothelium-derived
TY - JOUR. T1 - Effects of S-nitrosation and cross-linking of hemoglobin on hypoxic pulmonary vasoconstriction in isolated rat lungs. AU - Deem, Steven. AU - Kim, Joung Uk. AU - Manjula, Belur N.. AU - Acharya, A. Seetharama. AU - Kerr, Mark E.. AU - Patel, Rakesh P.. AU - Gladwin, Mark T.. AU - Swenson, Erik R.. PY - 2002/10/4. Y1 - 2002/10/4. N2 - Free hemoglobin (Hb) and red blood cells augment hypoxic pulmonary vasoconstriction (HPV) by scavenging nitric oxide (NO). S-nitrosation of Hb (SNO-Hb) may confer vasodilatory properties by allowing release of NO during deoxygenation and/or by interaction with small-molecular weight thiols. Likewise, cross-linking of free Hb may limit its vasoconstrictive effect by preventing abluminal movement of the molecule. We compared the effects of free SNO-Hb and Hb intramolecularly cross-linked at the β-cysteine 93 residue [Bis(maleidophenyl)-polyethylene glycol2000HbA (Bis-Mal-PEGHb)] to those of free oxyHb on pulmonary artery pressure (PAP), HPV, and ...
In isolated blood-perfused rat lungs, brief periods of ventilation hypoxia (2% O2) produce pulmonary vasoconstriction. In isolated lungs perfused with a salt-albumin solution, hypoxia produces no pulmonary vasoconstrictor responses in most preparations and only minimal responses in others. Vasoactive agents including angiotensin II, phenylephrine, epinephrine, norepinephrine, bradykinin, histamine, serotonin, and methoxamine were added to the salt-albumin perfusate to determine which substance, if any, was necessary for a pulmonary vasoconstrictor response during hypoxia. The addition of angiotensin II (12-120 nM) to the perfusate during hypoxia resulted in marked pulmonary vasoconstriction in proportion to the amount of angiotensin II added (a maximal response to hypoxia occurred with 120 nM angiotensin II). None of the other agents had the same effect, nor was their vasoactivity dependent on angiotensin II. Angiotensin II augmented the hypoxic response in doses that are themselves subpressor; ...
BACKGROUND: Hypoxic pulmonary vasoconstriction (HPV) is a defense mechanism to maintain adequate oxygenation. It has been reported that metabolism inhibition augments HPV. The purpose of the present study was, therefore, to determine the effect of metabolism inhibition on HPV in a rabbit model of isolated lung perfusion with exclusion of the influential factors on HPV. METHODS: In adult rabbits, lungs were isolated and perfused with a constant pulmonary perfusate flow. Acid-base status and temperature of perfusate was also constantly maintained. Thirty minutes after, the baseline hypoxic pressor response (HPR) was measured as the difference of pulmonary artery pressure (PAP) between a period of 21% normoxic gas inhalation and that of 3% hypoxic gas inhalation. After another thirty minutes, 2-deoxy-D-glucose 100 mg was mixed with the perfusate, and then HPR was measured three times. After checking metabolism inhibition effects, D-glucose 300 mg was mixed to the perfusate to reverse metabolism ...
TY - JOUR. T1 - Gender differences in the effect of age on electrical field stimulation (EFS)-induced adrenergic vasoconstriction in rat mesenteric resistance arteries. AU - Sullivan, Jennifer C. AU - Davison, Cathy A.. PY - 2001/3/14. Y1 - 2001/3/14. N2 - The objective of this study was to examine the effects of gender and age on electrical field stimulation (EFS)-induced vasoconstriction. Fisher 344 rats were studied: young females (YF, n = 38), young males (YM, n = 29), old females (OF, n = 33), and old males (OM, n = 30). Isolated mesenteric resistance arteries (endothelium-intact or denuded) were pressurized, and outer diameter was monitored. Dose-response curves were performed to KCl and phenylephrine (PE). EFS (0.1-16 Hz) responses were expressed as percentage of constriction from baseline. Area under the curve (AUC) was calculated and comparisons were made using analysis of variance and t tests. Females became less responsive to EFS-induced constriction with age, whereas constrictor ...
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We investigated the possible contributions of reactive oxygen species and of viscosity changes to hemodilution-induced inhibition of hypoxic pulmonary vasoconstriction (HPV) in dogs. Fourteen isoflurane-anesthetized dogs were randomly assigned to receive N-acetylcysteine (NAC) 200 mg/kg IV (n = 7) or placebo (n = 7). Mean pulmonary artery pressure (Ppa) was measured with cardiac output maintained constant by a manipulation of venous return in hyperoxia (fraction of inspired oxygen, 0.4) and in hypoxia (fraction of inspired oxygen, 0.1) at baseline and after stepwise reductions in hematocrit from 40% to 20%. Measured Ppa was compared with predicted Ppa by using a viscoelastic model. HPV was expressed as hypoxic Ppa minus hyperoxic Ppa. Hemodilution was associated with a decrease in HPV from 7 ± 1 mm Hg to 3 ± 1 mm Hg (P , 0.01), and this was completely prevented by NAC (HPV was unchanged, from 8 ± 1 to 8 ± 1 mm Hg; not significant). Hemodilution in the model decreased HPV from 8 ± 1 mm Hg to ...
TY - JOUR. T1 - The LKB1-AMPK-α1 signalling pathway triggers hypoxic pulmonary vasoconstriction downstream of mitochondria. AU - Moral-Sanz, Javier. AU - Lewis, Sophronia A.. AU - MacMillan, Sandy. AU - Ross, Fiona A.. AU - Thomson, Adrian. AU - Viollet, Benoit. AU - Foretz, Marc. AU - Moran, Carmel. AU - Hardie, D. Grahame. AU - Evans, A. Mark. PY - 2018/10/2. Y1 - 2018/10/2. U2 - 10.1126/scisignal.aau0296. DO - 10.1126/scisignal.aau0296. M3 - Article. VL - 11. JO - Science Signaling. JF - Science Signaling. SN - 1945-0877. IS - 550. ER - ...
Studies performed in our laboratory in conscious animals, demonstrate that the responsiveness of α-adrenergic receptors on the arterial vasculature of skeletal muscle is reduced during dynamic exercise compared to rest. A classical view of sympathetic vasoconstriction describes the release of norepinephrine (NE) which binds postsynaptic α-adrenergic receptors. There are two distinct populations of α-adrenergic receptors (α1 and α2) found of vascular smooth muscle, both of which produce vasoconstriction when stimulated. We have shown an attenuation of vasoconstriction during exercise with simultaneous stimulation of both populations of receptors. When examining the contribution of α1 and α2 receptors individually, α2 receptors appear to be much more sensitive to attenuation by exercise than α1 receptors. Existing evidence suggests that ATP acts as a neurotransmitter in vascular smooth muscle and is co-released with norepinephrine from sympathetic nerves. Recently we have examined P2X ...
Synonyms for vasoconstriction in Free Thesaurus. Antonyms for vasoconstriction. 1 word related to vasoconstriction: constriction. What are synonyms for vasoconstriction?
The results of the present study demonstrate that 20-HETE is produced by rat cerebral microvessels, and immunoreactive protein and mRNA for P-450 4A1, 4A2, 4A3, and 4A8 isoforms are expressed in these vessels. Subsequent GC/MS analysis confirmed the presence of 20-HETE in cerebral arteries and that an elevation in the transmural pressure from 20 to 140 mm Hg increased 20-HETE concentration in these vessels by 6-fold. The rise in 20-HETE concentration with elevation in transmural pressure suggests a role for this endogenous vasoconstrictor in the generation of pressure-induced cerebral vasoconstriction. Our findings that inhibitors of the formation of 20-HETE or blockers of its vasoconstrictor action eliminate the pressure-induced constriction of isolated cerebral arteries indicate that endogenous 20-HETE is an important component of pressure-induced cerebral arterial constriction. The idea that 20-HETE plays an important role in autoregulation of CBF is further supported by the observation that ...
Definition of vasoconstriction in the dictionary. Meaning of vasoconstriction. What does vasoconstriction mean? Information and translations of vasoconstriction in the most comprehensive dictionary definitions resource on the web.
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TY - JOUR. T1 - Angiotensin II stimulates internalization and degradation of arterial myocyte plasma membrane BK channels to induce vasoconstriction. AU - Leo, Marie Dennis. AU - Bulley, Simon. AU - Bannister, John P.. AU - Pushpamangalam Kuruvilla, Korah. AU - Narayanan, Damodaran. AU - Jaggar, Jonathan. PY - 2015/9/15. Y1 - 2015/9/15. N2 - Arterial smooth muscle cells (myocytes) express large-conductance Ca2+- activated K+ (BK) channel α and auxiliary β1 subunits that modulate arterial contractility. In arterial myocytes, β1 subunits are stored within highly mobile rab11A-positive recycling endosomes. In contrast, BKα subunits are primarily plasma membrane-localized. Trafficking pathways for BKα and whether physiological stimuli that regulate arterial contractility alter BKα localization in arterial myocytes are unclear. Here, using biotinylation, immunofluorescence resonance energy transfer (immunoFRET) microscopy, and RNAimediated knockdown, we demonstrate that rab4A-positive early ...
There does not need to be a change in circulating blood volume during exercise; the role of vasoconstriction is more subtle than that.. Vasoconstriction increases the stiffness of venous vessels leading back to the heart. This makes them act more like stiff tubes than elastic reservoirs. As a result, any extra blood pumped by the heart is more likely to return to the heart rather than to be stored in the venous vasculature. The importance of regulating venous return in concert with cardiac function has been appreciated at least since the work of Guyton and colleagues in the 1950s.. In exercise the effective muscle pump arising from the combination of muscle contraction and valves in the veins preventing backflow is also important; both the muscle pump and venoconstriction promote venous return to the heart.. ...
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Lipodema is a chronic disease of complex causes, many of which we understand little about. These include hormonal imbalance, an inability to metabolise exudate from blood vessels so that those proteins and cells that would normally be metabolised and returned to the circulation are deposited as adipose tissue in the subcutaneous tissue. The blood vessels themselves are affected, venous stasis and vasoconstriction occur and return is diminished especially at the subcutaneous level. This causes arterial constriction which accounts for the cold and often pale skin and leads to an increased lymphatic load(1). The condition worsens over years as tissue channels become progressively narrowed until the condition of a secondary lymphoedema, overlying the original lipodema, may lead to a situation where the patient may be either wheel-chair bound or bedridden. Weight gains can be up to or greater than 250 kgs. At this stage infections and intractable ulcers (or ones that necessitate skin grafts when lack ...
Vasoconstrictor -- [vas-oh-kuh n-strik-ter, vey-zoh-] noun, Physiology, Pharmacology: 1. a nerve or drug that causes vasoconstriction. Source:
Zhou Z, Hemradj V, de Beer VJ, Gao F, Hoekstra M, Merkus D, Duncker DJ. Cytochrome P-450 2C9 exerts a vasoconstrictor influence… Expand ...
Certain, they fully are. Nonetheless, heavy respiration reduces CO2 ranges within the blood and other cells and tissues. Since CO2 is basically probably the most highly effective acknowledged vasodilator, reduced CO2 degree causes vasoconstriction (or narrowing of blood vessels). This …. » Read more ...
In the early hours of the morning, near the end of the shift, I received a call to a 19 year-old male who was having an allergic reaction to his medicine. I arrived to find the man shivering in a chair and looking unwell. His friends were with him and they told me that he had brought medicine for a cold back from India where he had been recently and that he had started reacting to it. He had an erythemic rash but his airway seemed safe. His BP was a concern, however; it was consistently low - sometimes very low. When the crew arrived and we got him into the ambulance, we pondered this situation some more and I noticed that his feet were a little swollen and very red. I considered the possibility that the reaction was causing fluid pooling in his peripheries, which would explain his low BP. His legs were raised but this didnt help much, so I set up fluids and asked the crew to give him adrenaline, which would reverse the effects of histamine and nitric oxide and cause vasoconstriction, which in ...
Endothelial dysfunction plays a major role in ischemic cardiovascular disease, hypertension and cerebrovascular disease. Endothelium (inner lining of blood vessels) produces chemicals which result in relaxation of blood vessel muscles so the blood vessels can dilate. Also, produced are chemicals which cause the blood vessels to constrict. An imbalance in this dilation and constriction can […]. View Post ...
TY - JOUR. T1 - Characterization of the inhibitory effect of vascular endothelium on agonist-induced vasoconstriction in rat mesenteric resistance arteries. AU - Jin, Xin. AU - Satoh-Otonashi, Yukiko. AU - Zamami, Yoshito. AU - Koyama, Toshihiro. AU - Sun, Pengyuan. AU - Kitamura, Yoshihisa. AU - Kawasaki, Hiromu. N1 - Copyright: Copyright 2008 Elsevier B.V., All rights reserved.. PY - 2008. Y1 - 2008. N2 - Vascular endothelium regulates vascular tone by releasing endothelium-derived vasoactive substances. We performed this study to characterize the inhibitory effect of the endothelium on vasoconstrictor stimuli in rat mesenteric vascular beds. Changes in perfusion pressure induced by continuous perfusion of Krebs solution containing methoxamine (α1-adrenoceptor agonist) or high KCl were measured over 180 min. In preparations with intact endothelium, methoxamine-induced vasoconstriction was time-dependently decreased to cause 60% - 80% reduction of the initial vasoconstriction level, while no ...
To determine whether balloon angioplasty can provoke arterial vasoconstriction independent of platelet aggregation and neurogenic input, we studied the spontaneous vasomotor effects of balloon dilatation in isolated, perfused whole-vessel segments of rabbit aorta and pig carotid artery. Freshly dissected rabbit thoracic aortas were mounted in a muscle bath-perfusion chamber, perfused with physiologic saline solution at 70 mm Hg, and allowed to equilibrate. The proximal or distal half of the aortas were dilated with either a large (5 mm, 31-51% stretch beyond relaxed diameter) or a small (4 mm, 5-16% stretch) balloon angioplasty catheter with the other half of the vessel serving as the control. A similar series of experiments were performed in pig carotid arteries using large (6 or 8 mm, 48-90% stretch) balloon catheters. The spontaneous vasomotor effects of balloon angioplasty were examined with long-axis, high-frequency ultrasonic imaging combined with computerized edge detection image ...
TY - JOUR. T1 - Endothelin B receptor deficiency potentiates ET-1 and hypoxic pulmonary vasoconstriction. AU - Ivy, D. Dunbar. AU - Mcmurtry, Ivan F.. AU - Yanagisawa, Masashi. AU - Gariepy, Cheryl E.. AU - Le Cras, Timothy D.. AU - Gebb, Sarah A.. AU - Morris, Kenneth G.. AU - Wiseman, Richard C.. AU - Abman, Steven H.. PY - 2001/5. Y1 - 2001/5. N2 - Endothelin (ET)-1 contributes to the regulation of pulmonary vascular tone by stimulation of the ETA and ETB receptors. Although activation of the ETA receptor causes vasoconstriction, stimulation of the ETB receptors can elicit either vasodilation or vasoconstriction. To examine the physiological role of the ETB receptor in the pulmonary circulation, we studied a genetic rat model of ETB receptor deficiency [transgenic(sl/sl)]. We hypothesized that deficiency of the ETB receptor would predispose the transgenic(sl/sl) rat lung circulation to enhanced pulmonary vasoconstriction. We found that the lungs of transgenic(sl/sl) rats are ETB deficient ...
Hypoxic pulmonary vasoconstriction was originally described in 1946, by Von Euler and Liljestrand - they were studying the effects of hypoxic gas mixtures, and found that PA pressures increased with 10.5% inspired O2 [Von Euler and Liljestrand. Acta Physiol Scand 12: 301, 1946]. Since then, HPV has been well-described in multiple mammalian models, including humans. It is thought to result from a pathway involving NO and/or COOX inhibition [Moudgil R et al. J Appl Physiol 98: 390, 2005]. HPV takes effect over 30 minutes, although peak effect takes up to two hours. Interestingly, HPV sensitization occurs, in which a second incidence of hypoxemia produces a more significant response than the first [Dorrington KL et al. Am J Physiol Heart Circ Physiol 273, H1126, 1997] In addition to PAO2, HPV is dependent on both PaO2 and PvO2, although in the atelectatic lung only PvO2 matters and overall PAO2 is by far most important. Of note, HPV functions best when 30-70% of the lung is hypoxic - if , 30% of ...
Three inhibitors of the release or effects of endothelium-derived relaxing factor (EDRF), N-nitro-L-arginine, methylene blue and oxyhemoglobin, caused
Homocysteinemia is a major and independent risk factor for vascular disease. Oxidative stress is a possible mechanism for homocysteine (HCY)-induced vascular disease. Herein, we evaluated the antioxidant property of melatonin (MLT) in relation to the vasoconstrictive effect of HCY on the human umbilical artery. Helical umbilical arterial strips without endothelium were obtained at elective Cesarean delivery near term. Changes in potassium chloride (KCl)-induced vasoconstriction were measured. Arterial strips were treated with HCY (10 or 100 microM) plus FeSO(4) (10 microM) alone or pretreated with a hydroxyl radical ((*)OH) scavenger, mannitol (20 mM), or MLT (1 or 10 microM). The effect of HCY on the response of arterial strips to external calcium (Ca(2+)) in the presence of KCl (20 mM) was determined. HCY plus FeSO(4) potentiated KCl-induced vasoconstriction in a concentration-dependent manner; pretreatment with mannitol significantly reduced this vasospastic effect. HCY (100 microM) significantly
TRPV4 channel contributes to serotonin-induced pulmonary vasoconstriction and the enhanced vascular reactivity in chronic hypoxic pulmonary hypertension.
Small, muscular pulmonary arteries (PAs) constrict within seconds of the onset of alveolar hypoxia, diverting blood flow to better-ventilated lobes, thereby matching ventilation to perfusion and optimizing systemic PO2. This hypoxic pulmonary vasoconstriction (HPV) is enhanced by endothelial derived vasoconstrictors, such as endothelin, and inhibited by endothelial derived nitric oxide. However, the essence of the response is intrinsic to PA smooth muscle cells in resistance arteries (PASMCs). HPV is initiated by inhibition of the Kv channels in PASMCs which set the membrane potential (EM). It is currently uncertain whether this reflects an initial inhibitory effect of hypoxia on the K+ channels or an initial release of intracellular Ca2+, which then inhibits K+ channels. In either scenario, the resulting depolarization activates L-type, voltage gated Ca2+ channels, which raises cytosolic calcium levels [Ca2+]i and causes vasoconstriction. Nine families of Kv channels are recognized from cloning ...
The primary autonomic effects of amphetamines are on the vasculature and heart. Activation of alpha1 receptors can lead to significant vasoconstriction while at higher doses activation of beta1 receptors can increased heart rate and contractility. Together these effects can yield prominent systolic and diastolic hypertension. At toxic doses individuals may feel palpitations that can ultimately evolve into frank arrhythmias ...
It has repeatedly been shown that angiotensin II pretreatment enhances the subsequent hypoxic pressor responses in preparations perfused with artificial
Responses to angiotensin II were also depressed in adrenalectomized rats (Figure 2). Bolus angiotensin injections in isolated lungs produced typical transient
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Other articles where Vasoconstriction is discussed: cardiovascular disease: Vasoconstriction: Raynaud syndrome is said to occur when the extremities-primarily the fingers and toes but also including occasionally even the ears, nose, or cheeks-become pale, cyanotic, and numb under the influence of cold or emotion. Pain is also present at times. On cessation of the stimulus,…
Parenchymal arterioles (PAs) are high-resistance vessels in the brain that connect pial vessels to the microcirculation. We previously showed that PAs have increased vasoconstriction after ischemia and reperfusion that could increase perfusion defici
The primary novel finding of the present study is that sympathetic vasoconstrictor tone of the lower limb (i.e., leg) is augmented in old compared with young women. Specifically, young women exhibit no detectable sympathetic vasoconstriction in their leg vasculature at rest. Conversely, there appears to be robust vasoconstriction in the resting lower limbs of older women. Collectively, these findings suggest that with advanced age there is an emergence of a sympathetic neural influence on leg vascular tone in women. These conclusions are based on the observation that acute sympathetic inhibition via carotid artery baroreceptor loading increased femoral artery vascular conductance (FVC; Fig. 1) ~21% in old women, whereas FVC was unchanged in the younger women with the same intervention.. It is well established that muscle sympathetic nerve activity (MSNA) is augmented with age in women (Ng et al. 1993; Matsukawa et al. 1998; Moreau et al. 2003; Narkiewicz et al. 2005; Hart et al. 2011; Barnes ...
Angiotensin II (Ang II) is one of the most potent vasoconstrictor substances, yet paradoxically. Ang II may dilate certain vascular beds via an undefined mechanism. Ang II-induced vasoconstriction is mediated by the AT1 receptor, whereas the relative expression and functional importance of the AT2 receptor in regulating vascular resistance and blood pressure are unknown. We now report that Ang II induces relaxation of mesenteric microvessels and that this vasodilatory response was unaffected by losartan, an AT1 receptor antagonist, but was inhibited by PD123.319. a selective antagonist of AT2 receptors. In addition, reverse transcriptase-polymerase chain reaction studies revealed high amounts of AT2 receptor mRNA in smooth muscle from these same microvessels. Ang II-induced relaxation was inhibited by either tetraethylammonium or iberiotoxin, suggesting involvement of the large-conductance, calcium- and voltage-activated potassium (BKCa) channel. Subsequent whole-cell and single-channel patch-clamp
Biology of Vascular Smooth Muscle: Vasoconstriction and Dilatation - ISBN: 9789811048104 - (ebook) - von Yuansheng Gao, Verlag: Springer
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 ...
O:13:\PanistOpenUrl\:36:{s:10:\\u0000*\u0000openUrl\;N;s:6:\\u0000*\u0000idc\;N;s:6:\\u0000*\u0000fmt\;s:7:\journal\;s:6:\\u0000*\u0000doi\;s:0:\\;s:6:\\u0000*\u0000pii\;s:0:\\;s:7:\\u0000*\u0000pmid\;s:0:\\;s:9:\\u0000*\u0000atitle\;s:119:\ADRENERGIC MECHANISMS DO NOT CONTRIBUTE TO SALT-INDUCED VASOCONSTRICTION IN STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RAT\;s:9:\\u0000*\u0000jtitle\;s:0:\\;s:9:\\u0000*\u0000stitle\;s:0:\\;s:7:\\u0000*\u0000date\;s:4:\1982\;s:9:\\u0000*\u0000volume\;s:0:\\;s:8:\\u0000*\u0000issue\;s:0:\\;s:8:\\u0000*\u0000spage\;s:0:\\;s:8:\\u0000*\u0000epage\;s:0:\\;s:8:\\u0000*\u0000pages\;s:0:\\;s:7:\\u0000*\u0000issn\;s:0:\\;s:8:\\u0000*\u0000eissn\;s:0:\\;s:9:\\u0000*\u0000aulast\;s:9:\TAKESHITA\;s:10:\\u0000*\u0000aufirst\;s:1:\A\;s:9:\\u0000*\u0000auinit\;N;s:10:\\u0000*\u0000auinitm\;N;s:5:\\u0000*\u0000au\;a:3:{i:0;s:10:\IMAIZUMI T\;i:1;s:10:\ASHIHARA T\;i:2;s:10:\NAKAMURA ...
Epinephrine acts on alpha receptors causing vasoconstriction and on beta receptors causing vasodilation. The affinity of epinephrine for beta receptors is somewhat greater than its affinity for alpha receptors. When given in low doses, or by slow IV infusion in humans, the beta effects of epinephrine may predominate. When given in a large IV bolus dose, as here, the alpha effects (vasoconstriction) predominate when the concentration of epinephrine is high, and the beta effects (vasodilation) may sometimes be seen as the concentration is falling. From these facts you may be able to infer the relative affinity of epinephrine for alpha receptors on the one hand, and beta receptors on the other hand.The fact that vasoconstriction predominates when both alpha and beta receptors are activated shows that the capacity for vasoconstriction mediated by alpha receptors is very great, whereas the capacity for vasodilation mediated by beta receptors is somewhat limited. ...
TY - ABST. T1 - N-Acetylcysteine Attenuates Aldosterone induced Vasoconstriction in Individuals with Type 2 Diabetes. AU - Finsen, Stine Louise Høyer. AU - Mortensen, Stefan. N1 - This event was canceled due to COVID-19.. PY - 2020. Y1 - 2020. U2 - 10.1096/fasebj.2020.34.s1.05400. DO - 10.1096/fasebj.2020.34.s1.05400. M3 - Conference abstract in journal. VL - 34. JO - F A S E B Journal. JF - F A S E B Journal. SN - 0892-6638. IS - Suppl. 1. Y2 - 4 April 2020 through 7 April 2020. ER - ...
• Extensively used in plastic surgery to produce vasoconstriction, which reduces blood loss during surgery, although there is some concern
Results Acetylcholine induced significant vasoconstrictive responses in the distal but not in the proximal segments of both the stented (-11 ± 7% versus baseline; p , .01) and the contralateral vessels (-11 ± 6%; p , .01), which were significantly correlated (R = .48; p , .05) and were completely reverted by nitroglycerine. Inducible ischemia was the only predictive factor for distal vasoconstriction in the stented vessel (p , .01) but not in the contralateral vessel (p = .06). Patients with minor signs of ischemia at the ergometric test showed a greater vasoconstriction than those with a completely normal test (-16 ± 7% versus -7 ± 6%; p , .01). ...
A preparation was devised in which the sympathetic vasoconstrictor response in the dog kidney perfused in vivo at constant blood flow could be elicited and measured, and the accompanying release of transmitter into the venous effluent could be quantitated. An i.a. infusion of angiotensin II amide resulted in potentiation of the response to sympathetic stimulation at a low frequency (2 cps) and an increased release of catecholamine elicited during stimulation at a higher frequency (5 cps). The vasoconstrictor response to sympathetic stimulation was increased to a much greater degree than the vasoconstrictor response to i.a. administered norepinephnine (1 µg). Cocaine, when infused i.a., potentiated the responses to both sympathetic stimulation and norepinephrine, the latter to a somewhat greater degree. Release of catecholamine during stimulation at the higher frequency also was increased after cocaine. The difference in the relative degree of potentiation of the response to endogenously ...
The active agents like Aldoril 25 which specifically causes vasoconstriction in every brain veins help himself get over the increased sensitivity of skin ...
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS ...
The major findings of this study are that blockade of NOS with L‐NAME (but not with the iNOS inhibitor L‐canavanine) caused marked increases in the already elevated RVSP at 3, 5, and 8 weeks after the initiation of the SU/Hx/Nx‐induced PAH in rats that simulate the human PAH phenotype histologically as well as hemodynamically (Abe et al. 2010; Toba et al. 2014). The increases in RVSP in response to L‐NAME were apparently caused by active pulmonary vasoconstriction since they were not accompanied by increases in cardiac output. In contrast, NOS inhibition did not increase the elevated RVSP nor decrease the CI at an earlier time point (1 week after the initiation) of this PAH model. It has previously been shown that Rho kinase‐mediated vasoconstriction contributes markedly to the high RVSP and TPRI throughout the PAH process, that is, from the early (1‐week) to the late (13‐week time point) in SU/Hx/Nx rats (Oka et al. 2007; Toba et al. 2014). It is therefore speculated that at late ...
I had a heart attack in the beginning of October of this year (confirmed by elevated cardiac enzymes) and in the angiogram (sp) they did not find a blockage but were able to see where the damage was an...
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Acetylcholine, Animal, Animal Model, Atherosclerosis, Cardiovascular Disease, Depression, Disease, Endothelium, Mice, Patients, Phenylephrine, Procedure, Risk, Risk Factor, Vasoconstriction, Vasorelaxation
Adults, Aging, Air, Elderly, Productivity, Sensation, Skin, Skin Temperature, Temperature, Transient, Vasoconstriction, Young Adults
... Transmission electron micrograph showing vasoconstriction of a microvessel by pericytes and endothelial cells ... Medications that cause vasoconstriction include: antihistamines, decongestants, and stimulants. Severe vasoconstriction may ... Vasoconstriction can be a contributing factor to erectile dysfunction.[7] An increase in blood flow to the penis causes an ... Vasoconstriction is a procedure of the body that averts orthostatic hypotension. It is a part of a body negative feedback loop ...
VasoconstrictionEdit. IP receptor agonists are front-line drugs to treat pulmonary hypertension. Major drugs in this category ... IP agonists are also to treat severe vasoconstriction in Raynaud's disease, Raynaud's disease-like syndromes, and scleroderma.[ ... IP agonists are used to treat patients pathological vasoconstriction diseases.[15] The injection of IP activators into the skin ... stimulators of IP are used to treat severe and even life-threatening diseases involving pathological vasoconstriction. ...
Vasoconstriction and vasodilationEdit. Immediately after a blood vessel is breached, ruptured cell membranes release ... This vasoconstriction lasts five to ten minutes and is followed by vasodilation, a widening of blood vessels, which peaks at ...
vasoconstriction and mydriasis; used as vasopressors, nasal decongestants and during eye exams). Selected examples are: ...
"Vasodilation and Vasoconstriction: Real Story." Vasodilation and Vasoconstriction. 2011. Web. 21 May 2012. University of ... Decreases and increases in temperature trigger vasoconstriction and vasodilation respectively. Vasoconstriction affects flow ... Like vasoconstriction, vasodilation can be caused by internal and external factors. For example, nitric oxide, found in food, ... the opposite of vasoconstriction. In vasodilation the blood vessels dilate to allow more blood flow. The smooth muscle cells ...
Splanchnic-mesenteric vasoconstriction Splanchnic vasoconstriction Octreotide[92][93] Hypovolemic POTS Synthetic ... Splanchnic vasoconstriction. Increase blood pressure. Pyridostigmine[16][104][105] Other (Refractory POTS) Psychostimulant ... which may be beneficial not only by augmenting sympathetically-mediated vasoconstriction, but also because a large subset of ...
It occurs after vasoconstriction. During the process, platelets begin to accumulate, or aggregate, on the damaged vessel wall. ... As such, platelet plug formation occurs after vasoconstriction of the blood vessels but before the creation of the fibrin mesh ...
vasoconstriction, inhibits platelets. inactivating mutations in the 20-HETE-forming enzyme, CYP2U1, associated with Hereditary ... Many of the prostanoids are known to mediate local symptoms of inflammation: vasoconstriction or vasodilation, coagulation, ...
This process is called vasoconstriction. It is impossible to prevent all heat loss from the blood, only to reduce it. In ... extremely cold conditions, excessive vasoconstriction leads to numbness and pale skin. Frostbite occurs only when water within ...
The dry gangrene is a result of vasoconstriction induced by the ergotamine-ergocristine alkaloids of the fungus. It affects the ... Vasoconstriction is treated with vasodilators. Historically, eating grain products, particularly rye, contaminated with the ...
It involves vasoconstrictions of blood vessels connected to and within the lungs. As a result, the heart has a hard time ... Endothelial dysfunction induces coronary vasoconstriction. This is caused by catecholamine release and by infections. Severe ... which acts through yet to-be-determined mechanisms to induce vasoconstriction. It has also been shown that agonists of ...
Heat loss is also inhibited by the cocaine-induced vasoconstriction. Cocaine and/or associated hyperthermia may cause muscle ... Calcium channel blockers may also be used to treat hypertension and coronary arterial vasoconstriction, but fail to lower ... Cocaine and its metabolites may cause arterial vasoconstriction hours after use. Epicardial coronary arteries are especially ... The phenomenon of "unopposed alpha-stimulation," in which blood pressure increases or coronary artery vasoconstriction worsens ...
... refers to a condition in which an arterial spasm leads to vasoconstriction. This can lead to tissue ischemia and ...
Both of these factors affect pH and, in turn, the balance between vasodilation versus vasoconstriction in the brain. So, the ... Vasodilation Vasoconstriction Vascular resistance "CV Physiology , Local Regulation of Blood Flow". ... Pulmonary (lung) circulation undergoes hypoxic vasoconstriction, which is a unique mechanism of local regulation in that the ... endothelin-1 causes vasoconstriction. Below are several examples of differing types of local blood flow regulation by specific ...
... but in the brain alone it causes vasoconstriction (narrowing of the blood vessels)[citation needed]. This vasoconstriction ... Vasoconstriction is only reversed by the build-up of carbon dioxide in the blood through suspension of breathing. In some ... Increase in blood pH, (respiratory alkalosis). Vasoconstriction of blood vessels supplying brain. Pooling of the blood present ... it is highly vulnerable if vasoconstriction is not reversed. Normally, if the brain is hypoxic, autonomous systems in the body ...
This pathway typically involves regulating vasoconstriction. When vasopressin binds to AVPR1B, a GPCR, the phosphatidylinositol ...
Vasodilation and vasoconstriction are complex phenomena; they are functions not merely of the fluid mechanics of pressure and ...
The process is the opposite of vasoconstriction, which is the narrowing of blood vessels. When blood vessels dilate, the flow ... The spinal cord has both vasodilation and vasoconstriction nerves. The neurons that control vascular vasodilation originate in ... The opposite physiological process is vasoconstriction. These processes are naturally modulated by local paracrine agents from ... Charkoudian, Nisha (2010). "Mechanisms and modifiers of reflex induced cutaneous vasodilation and vasoconstriction in humans". ...
ani, C., Gopher, D., Lavie, P. (2004). Peripheral vasoconstriction reflects exerted mental effort. Psychophysiology, 41, pp 789 ...
Sessler DI, Moayeri A, Støen R, Glosten B, Hynson J, McGuire J (1990). "Thermoregulatory vasoconstriction decreases cutaneous ... In essence, hypothermia increases preglomerular vasoconstriction, thus decreasing both renal blood flow (RBF) and GFR. Accurate ...
Enables clotting; releases serotonin which causes vasoconstriction Red blood cells[edit]. Red and white human blood cells as ...
This insight resulted in bedside tests for nerve damage and vasoconstriction. Wrinkling is often scored with immersion of the ... Einar P.V. Wilder-Smith; Adeline Chow (2003). "Water-immersion wrinkeling is due to vasoconstriction". Muscle & Nerve. 27 (3): ... Recent research shows that wrinkling is related to vasoconstriction. Water probably initiates the wrinkling process by altering ...
Arginine Hypertension Protein detoxification Vasoconstriction Vallance, P.; Leone, A.; Calver, A.; Collier, J.; Moncada, S. ( ...
This phenomenon is called hypoxic pulmonary vasoconstriction and it is initially a protective response designed to stop too ... When the alveolar hypoxia is widespread and prolonged, this hypoxia-mediated vasoconstriction occurs across a large portion of ... Plasma levels of serotonin, which promotes vasoconstriction, hypertrophy and proliferation, are increased in patients with PAH ... The mechanisms involved in this narrowing process include vasoconstriction, thrombosis, and vascular remodeling (excessive ...
... angiotensin II causes vasoconstriction and aldosterone release. Aldosterone serves to retain sodium from the distal renal ...
Vasoconstriction Vasodilation Vasospasm Haddock RE, Hill CE. Rhythmicity in arterial smooth muscle. J Physiol (Lond ). 2005; ...
Vasoconstriction is the correct word here.). *(diff , hist) . . Cannibal Holocaust‎; 16:42 . . (+32)‎ . . ‎. Little Bizarre Dio ...
When chewed it can cause palpitation and vasoconstriction. This form is eaten in the lower regions of Bhutan and in North ...
It blocks thromboxane induced platelet aggregation and vasoconstriction. Waksman R, Gurbel P, Gaglia M (2014). Antiplatelet ...
Tayefeh F; Plattner O; Sessler DI; Ikeda T; Marder D. (February 1998). "Circadian changes in the sweating-to-vasoconstriction ... Matsukawa T, Kurz A, Sessler DI, Bjorksten AR, Merrifield B, Cheng C (1995). "Propofol linearly reduces the vasoconstriction ... De Witte JL, Kim JS, Sessler DI, Bastanmehr H, Björksten AR (1998). "Tramadol reduces the sweating, vasoconstriction, and ... vasoconstriction, and shivering thresholds in humans". Anesthesiology. 80 (4): 780-8. doi:10.1097/00000542-199404000-00009. ...
Vasoconstriction. Transmission electron micrograph showing vasoconstriction of a microvessel by pericytes and endothelial cells ... Medications that cause vasoconstriction include: antihistamines, decongestants, and stimulants. Severe vasoconstriction may ... Ambient temperature is an example of exogenous vasoconstriction. Cutaneous vasoconstriction will occur because of the bodys ... Vasoconstriction can be a contributing factor to erectile dysfunction.[8] An increase in blood flow to the penis causes an ...
Vasoconstriction: Raynaud syndrome is said to occur when the extremities-primarily the fingers and toes but also including ... Other articles where Vasoconstriction is discussed: cardiovascular disease: ... In cardiovascular disease: Vasoconstriction. Raynaud syndrome is said to occur when the extremities-primarily the fingers and ... blood pressure in mammals through vasoconstriction (i.e., contraction of blood vessels), this action requires a high ...
Vasoconstriction is the narrowing (constriction) of blood vessels by small muscles in their walls. When blood vessels constrict ... Vasoconstriction may be slight or severe. It may result from disease, drugs, or psychological conditions. Medicines that cause ... Vasoconstriction is the narrowing (constriction) of blood vessels by small muscles in their walls. When blood vessels constrict ... Medicines may be used to increase or reduce vasoconstriction in very ill people. ...
Hypoxic pulmonary vasoconstriction.. Marshall BE1.. Author information. 1. University of Pennsylvania Medical School, ...
Medications may be used to treat vasoconstriction or to cause ... Vasoconstriction is constriction or narrowing of a blood vessel ... Vasoconstriction is constriction or narrowing of a blood vessel. When a blood vessel constricts, the flow of blood is ...
血管收縮(vasoconstriction),亦即血管收窄,是指體內血管管腔收窄,這會造成血壓的上升。它的相反過程稱為血管舒張。 血管收縮可以是由血管收縮劑造成。血管收縮劑是針對特定的受體,如抗利尿激素受體或腎上腺素受體。血管收縮劑亦會在臨床使用增加血壓 ... 血管收縮
We discuss whats happening and why its normal, what causes vasoconstriction to become disordered, and when vasoconstriction ... Vasoconstriction is a normal and complex process where blood vessels in your body narrow, restricting blood flow from an area. ...
Reversible cerebral vasoconstriction syndrome (RCVS, sometimes called Call-Fleming syndrome) is a disease characterized by a ... Less than 5% of patients experience progressive vasoconstriction, which can lead to stroke, progressive cerebral edema, or even ... A 2007 review by Leonard Calabrese and colleagues proposed the name reversible cerebral vasoconstriction syndrome, which has ... Mehdi, A. & Hajj-Ali, R. A. (2014). "Reversible cerebral vasoconstriction syndrome: a comprehensive update". Current Pain and ...
Vasoconstriction. Transmission electron micrograph showing vasoconstriction of a microvessel by pericytes and endothelial cells ... Medications that cause vasoconstriction include: antihistamines, decongestants, and stimulants. Severe vasoconstriction may ... Vasoconstriction can be a contributing factor to erectile dysfunction.[7] An increase in blood flow to the penis causes an ... Vasoconstriction is a procedure of the body that averts orthostatic hypotension. It is a part of a body negative feedback loop ...
Heart Attack from VasoConstriction syralia I had a heart attack in the beginning of October of this year (confirmed by elevated ... Heart Attack from VasoConstriction. I had a heart attack in the beginning of October of this year (confirmed by elevated ... My question is... since I have already had a heart attack from vasoconstriction am I more likely to have another from it? ... My question is... since I have already had a heart attack from vasoconstriction am I more likely to have another from it? ...
To determine whether epinephrine facilitates neurogenic vasoconstriction in humans, we contrasted forearm vasoconstrictor ... provide the first hemodynamic evidence in humans that epinephrine and isoproterenol facilitate neurogenic vasoconstriction. The ...
encoded search term (What is the role of endothelial cells in cocaine-induced vasoconstriction?) and What is the role of ... What is the role of endothelial cells in cocaine-induced vasoconstriction?. Updated: Sep 01, 2018 ... In patients with dysfunctional endothelium, serotonin causes intense vasoconstriction because of its unopposed effects on ... and animal studies suggest that endothelial dysfunction predisposes a person to vasoconstriction and arterial spasm. ...
Reversible cerebral vasoconstriction syndromes: analysis of 139 cases.. Singhal AB1, Hajj-Ali RA, Topcuoglu MA, Fok J, Bena J, ... Reversible cerebral vasoconstriction syndrome: a rose by any other name? [Arch Neurol. 2011] ... Reversible cerebral vasoconstriction syndrome and hemorrhagic events: who precedes whom? [Arch Neurol. 2011] ... One hundred thirty-nine patients with reversible cerebral vasoconstriction syndromes.. MAIN OUTCOME MEASURES: Clinical, ...
23 patients with reversible cerebral vasoconstriction syndrome experience fatigue, depressed mood, pain, anxious mood, and ... Find the most comprehensive real-world symptom and treatment data on reversible cerebral vasoconstriction syndrome at ... and Medical marijuana to treat their reversible cerebral vasoconstriction syndrome and its symptoms. ... 4 reversible cerebral vasoconstriction syndrome patients report severe fatigue (66%). * 2 reversible cerebral vasoconstriction ...
Endothelium-dependent arterial vasoconstriction after balloon angioplasty.. T A Fischell, U Nellessen, D E Johnson, R Ginsburg ... Endothelium-dependent arterial vasoconstriction after balloon angioplasty.. T A Fischell, U Nellessen, D E Johnson and R ... Endothelium-dependent arterial vasoconstriction after balloon angioplasty.. T A Fischell, U Nellessen, D E Johnson and R ... and calcium-channel blockade in modulating angioplasty-induced vasoconstriction. Significant arterial vasoconstriction was ...
... of the local anesthetic-induced maximum vasoconstriction. We determined the order of potency (ED50) of vasoconstriction among ... Aminoamide local anesthetics induce vasoconstriction in vivo and in vitro. The goals of this in vitro study were to investigate ... Vasoconstriction Potency Induced by Aminoamide Local Anesthetics Correlates with Lipid Solubility. Hui-Jin Sung,1 Seong-Ho Ok,2 ... The potency of the vasoconstriction in the endothelium-denuded aorta induced by local anesthetics is determined primarily by ...
... local anesthetic concentration producing maximal vasoconstriction] =. −. 0. .. 4. 6. 1. −. 1. .. 4. 0. 7. ×. l. o. g. 𝑃. ; 𝑟. 2 ... of the local anesthetic-induced maximum vasoconstriction. We determined the order of potency (ED50) of vasoconstriction among ... Aminoamide local anesthetics induce vasoconstriction in vivo and in vitro. The goals of this in vitro study were to investigate ... Vasoconstriction Potency Induced by Aminoamide Local Anesthetics Correlates with Lipid Solubility. Hui-Jin Sung,1 Seong-Ho Ok,2 ...
Hypoxic pulmonary vasoconstriction. J Appl Physiol. 2005;98(1):390-403.. View this article via: PubMed CrossRef Google Scholar ... Activation of Toll-like receptor 2 impairs hypoxic pulmonary vasoconstriction in mice. Am J Physiol Lung Cell Mol Physiol. 2008 ... Hypoxic pulmonary vasoconstriction requires connexin 40-mediated endothelial signal conduction. Liming Wang,1,2,3,4 Jun Yin,1,2 ... Prominent role of intracellular Ca2+ release in hypoxic vasoconstriction of canine pulmonary artery. Br J Pharmacol. 1997;122(1 ...
... to the treatment and prevention of asthma or other forms of broncho-constriction or reversible pulmonary vasoconstriction in a ... or of reversible pulmonary vaso-constriction (i.e., acute pulmonary vasoconstriction or chronic pulmonary vasoconstriction ... Such vasoconstriction can lead to abnormally high blood pressure (hypertension) in the affected portion of the circulatory ... Conceptually analogous to the narrowing of the airways of the lung which occurs in an asthma attack, vasoconstriction is a ...
Increased AT1 receptor expression mediates vasoconstriction leading to hypertension in Snx1−/− mice. *Chao Liu1,2,3 na1, ... Liu, C., Li, X., Fu, J. et al. Increased AT1 receptor expression mediates vasoconstriction leading to hypertension in Snx1−/− ... leading to increased vasoconstriction and blood pressure. ... leading to increased vasoconstriction and blood pressure. ...
Conditions: Blood pressure, Hypernatremia (high sodium), Hypertension, Kidney disease, Potassium deficiency, Vasoconstriction, ... Conditions: Cardiovascular disease, Endothelial dysfunction, Hypertension, Vasoconstriction. *Supplements: Amino acids, ...
Coronary-artery vasoconstriction induced by cocaine, cigarette smoking, or both [9].. *The vasoconstriction is attenuated by ... Associations of Vasoconstriction with chemical compounds. *Inhibition of hypoxic pulmonary vasoconstriction by nifedipine [25]. ... Gene context of Vasoconstriction. *Vasoconstriction to endothelin-1 was abolished by co-infusion of BQ-123 (p = 0.006), with ... Chemical compound and disease context of Vasoconstriction. *We have demonstrated paradoxical vasoconstriction induced by ...
Perfusion MRI in Reversible Cerebral Vasoconstriction Syndrome. The safety and scientific validity of this study is the ... Reversible Cerebral Vasoconstriction Syndrome Device: MRI brain Device: ASL-MRI brain Device: MRA brain ... Prevalence of radiological vasoconstriction seen on magnetic resonance angiography (MRA) in RCVS is reported to be between 60- ... Reversible cerebral vasoconstriction syndrome. Intern Med J. 2015 Jun;45(6):599-608. doi: 10.1111/imj.12669. Review. ...
... N Engl J Med. 1989 Dec 7;321(23):1557-62. doi: 10.1056/NEJM198912073212301. ... We conclude that the intranasal administration of cocaine near the dose used for topical anesthesia causes vasoconstriction of ...
A vasoconstriction response to acute severe hypertension is likely to explain this reversible angiopathy. ... Postpartum cerebral angiopathy: reversible vasoconstriction assessed by transcranial Doppler ultrasounds Eur Neurol. 1989;29(2 ...
We tested for a nonnoradrenergic mechanism of reflex cutaneous vasoconstriction with whole body progressive cooling in seven ... During cooling, vasoconstriction was blocked at BT sites (P , 0.05). CVC at saline sites fell significantly beginning at T(SK) ... We tested for a nonnoradrenergic mechanism of reflex cutaneous vasoconstriction with whole body progressive cooling in seven ... Because the effects of NE were blocked at sites showing significant reflex vasoconstriction, a nonnoradrenergic mechanism in ...
Coronary artery spasm and vasoconstriction. The case for a distinction.. A Maseri, G Davies, D Hackett, J C Kaski ...
Deletion of G Protein-Coupled Estrogen Receptor Increases Endothelial Vasoconstriction. Matthias R. Meyer, Kerstin Amann, ... Obesity and risk of vascular disease: importance of endothelium-derived vasoconstriction. Br J Pharmacol. Epub ahead of print ... Deletion of G Protein-Coupled Estrogen Receptor Increases Endothelial Vasoconstriction. Matthias R. Meyer, Kerstin Amann, ... Deletion of G Protein-Coupled Estrogen Receptor Increases Endothelial Vasoconstriction. Matthias R. Meyer, Kerstin Amann, ...
  • For example, vasoconstriction is a hypothermic preventative in which the blood vessels constrict and blood must move at a higher pressure to actively prevent a hypoxic reaction. (
  • Hypoxic pulmonary vasoconstriction. (
  • The effects of endothelin receptor blockade on the pulmonary circulation have been reported variably, possibly in relation to a more or less important associated release of endogenous nitric oxide (NO). The aim of this study was to test whether endothelin antagonism would inhibit hypoxic pulmonary vasoconstriction, and if it would not, then would it do so after NO synthase inhibition. (
  • Hypoxic pulmonary vasoconstriction (HPV) was evaluated in anesthetised dogs by the increase in the mean pulmonary artery pressure ( P pa ) minus occluded P pa ( P pao ) gradient in response to hypoxia (inspiratory oxygen fraction of 0.1) at constant pulmonary blood flow. (
  • The authors conclude that endogenous nitric oxide is released by, and opposes the vasoconstricting effects of, endothelins in vivo , reducing systemic blood pressure and limiting hypoxic pulmonary vasoconstriction. (
  • Endothelins have been hypothesised to play a role in the mediation of hypoxic pulmonary vasoconstriction (HPV). (
  • Complete reference on hypoxic pulmonary vasoconstriction and hypoxia-mediated pulmonary hypertension. (
  • 1. To test whether almitrine might improve the arterial partial pressure of O 2 in patients with chronic obstructive airways disease by improvement of ventilation-perfusion matching, we looked at the interaction between hypoxic and almitrine-induced vasoconstriction in isolated rat lungs perfused with blood at constant flow. (
  • 2. Almitrine, given in increasing doses between challenges with 2% O 2 , enhanced hypoxic vasoconstriction at low doses but attenuated it at high doses. (
  • 8. Almitrine-induced vasoconstriction was attenuated by a fall in perfusate temperature in a similar manner to hypoxic vasoconstriction. (
  • It was also attenuated by three drugs, chlorpheniramine, propanolol and diethylcarbamazine, all of which also decrease hypoxic vasoconstriction. (
  • The similarity between hypoxic and almitrine-induced pulmonary vasoconstriction is further confirmed. (
  • Notch Activation of Ca(2+) Signaling in the Development of Hypoxic Pulmonary Vasoconstriction and Pulmonary Hypertension. (
  • Hypoxic pulmonary vasoconstriction (HPV) is an important physiological response that optimizes the ventilation/perfusion ratio. (
  • BACKGROUND: Hypoxic pulmonary vasoconstriction (HPV) is a defense mechanism to maintain adequate oxygenation. (
  • Additionally, the requirement of functional mitochondrial complex II for hypoxic pulmonary vasoconstriction was determined by videomorphometric analysis of small intrapulmonary vessels in precision cut lung slices. (
  • Hypoxic pulmonary vasoconstriction was originally described in 1946, by Von Euler and Liljestrand - they were studying the effects of hypoxic gas mixtures, and found that PA pressures increased with 10.5% inspired O2 [Von Euler and Liljestrand. (
  • Reversible cerebral vasoconstriction syndrome (RCVS, sometimes called Call-Fleming syndrome) is a disease characterized by a weeks-long course of thunderclap headaches, sometimes focal neurologic signs, and occasionally seizures. (
  • Reversible cerebral vasoconstriction syndrome: a rose by any other name? (
  • Reversible cerebral vasoconstriction syndrome and hemorrhagic events: who precedes whom? (
  • Reversible cerebral vasoconstriction syndrome is characterized by recurrent acute severe headaches, and multiple areas of narrowing (constriction) of blood vessels within the brain. (
  • Data from patients with reversible cerebral vasoconstriction syndrome, who reported starting treatments within the last 5 years. (
  • Reversible Cerebral Vasoconstriction Syndrome (RCVS) is a group of conditions characterised by prolonged but reversible multifocal narrowing of the cerebral arteries. (
  • depending on the degree of vasoconstriction, RCVS may be associated with cortical subarachnoid haemorrhage (in approximately 34% of patients), ischaemic infarction (6-39% of patients), or concomitant posterior reversible encephalopathy syndrome (PRES, 9-38% of patients). (
  • The authors report the case of a 67-year-old woman with reversible cerebral vasoconstriction syndrome (RCVS) who manifested symptoms of Bálint syndrome (simultagnosia, optic ataxia, and ocular apraxia) and visual allochiria in which visual stimuli presented to one hemispace are transposed to the opposite side. (
  • Speculated mechanisms include reperfusion injury attributable to vasodilatation after severe vasoconstriction or as a consequence of hypertension and disturbed autoregulation (as may occur in another poorly understood syndrome that overlaps with RCVS, posterior reversible encephalopathy syndrome). (
  • Vasodilator responses and endothelin-dependent vasoconstriction in metabolically healthy obesity and the metabolic syndrome. (
  • In this case of cerebral malaria, the MRA findings indicated the involvement of reversible cerebral vasoconstriction syndrome. (
  • Reversible cerebral vasoconstriction syndrome is a clinical and radiologic syndrome that represents a common presentation of a diverse group of disorders. (
  • The syndrome is characterized by thunderclap headache and reversible vasoconstriction of cerebral arteries, which can either be spontaneous or related to an exogenous trigger. (
  • The pathophysiology of reversible cerebral vasoconstriction syndrome is unknown, though alterations in cerebral vascular tone are thought to be a key underlying mechanism. (
  • however, reversible cerebral vasoconstriction syndrome may result in permanent disability or death in a small minority of patients secondary to complications such as ischemic stroke or intracranial hemorrhage. (
  • Reversible cerebral vasoconstriction syndrome (RCVS) is a clinical and radiologic syndrome whose primary features include the hyperacute onset of severe headache and segmental vasoconstriction of cerebral arteries that resolves by 3 months. (
  • Reversible cerebral vasoconstriction syndrome (RCVS) is a rare condition characterized by a sudden narrowing (constriction) of blood vessels that supply blood carrying oxygen and nutrients to the brain. (
  • The clinical and radiological spectrum of reversible cerebral vasoconstriction syndrome. (
  • Given her gradual increase of velocities and Lindegaard index, together with fixed left sensory and motor deficits, we performed CT angiography, which suggested cerebral vasoconstriction syndrome. (
  • Reversible cerebral vasoconstriction syndrome in puerperium: A prospective study. (
  • BACKGROUND AND AIM OF THE STUDY: Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by severe "thunderclap" headache, with or without associated neurological symptoms and neuroimaging findings of reversible vasoconstriction of cerebral arteries. (
  • Because NE induces vasoconstriction of rat aorta ( Alosachie and Godfraind, 1988 ), herein we used isolated rat aorta instead of bovine coronary artery. (
  • In the pulmonary vasculature hypoxia induces vasoconstriction and vascular remodelling. (
  • Direct electric current induces vasoconstriction and thrombosis [ 32 - 34 ] but also causes tissue damage. (
  • As NO is known to mask part of the renal effects of vasoconstrictor drugs, we queried whether the Ang II-induced vasoconstrictions could occur via multiple receptor subtypes during inhibition of NO synthesis. (
  • By contrast, PD-123319 (0.5-500 nM) did not affect the 10 nM Ang II-induced vasoconstriction and concentration-dependently decreased the 0.1 nM Ang II-induced vasoconstriction plateauing at 65% inhibition above 5 nM antagonist. (
  • 7. In conclusion, the renal Ang II-induced vasoconstriction, which is antagonized only by AT1-R antagonist in the presence of endogenous NO, becomes sensitive to both AT1- and AT2-R antagonists during NO synthesis inhibition. (
  • Effects of chronic PGHS-2 inhibition on PGHS-dependent vasoconstriction in the aged female rat. (
  • 5-HT-induced K + channel inhibition increases [Ca 2+ ] i in PASMCs, which is a major trigger for pulmonary vasoconstriction and development of pulmonary arterial hypertension (PAH). (
  • In conclusion, KMUP-1 ameliorates 5-HT-induced vasoconstriction and K + -channel inhibition through the PKC pathway, which could be valuable to prevent the development of PAH. (
  • The purpose of this study is to test the hypothesis that the stimulation of VSMC P2XR receptors (P2XRs) contributes to ATP-evoked sustained vasoconstrictions in rat middle cerebral arteries (RMCAs). (
  • MELAS and reversible vasoconstriction of the major cerebral arteries. (
  • A vasoconstriction response to acute severe hypertension is likely to explain this reversible angiopathy. (
  • RCVS is diagnosed by detecting diffuse reversible cerebral vasoconstriction. (
  • This study aims to quantify perfusion, assess arterial vasoconstriction, and confirm reversibility using 3T ASL-MRI and MRA in 10 patients with suspected RCVS. (
  • Acquiring these data at multiple time points during RCVS progression, the investigators will assess the relationship between vasoconstriction and downstream perfusion and determine the role of these imaging techniques in early and accurate diagnosis of RCVS. (
  • The hallmark of RCVS is vasoconstriction seen on vascular imaging scans and typically reverses within 3 months. (
  • Prevalence of radiological vasoconstriction seen on magnetic resonance angiography (MRA) in RCVS is reported to be between 60-90% and typically appears as diffuse segmental constriction of large and medium sized vessels lasting 4-12 weeks. (
  • 1 ⇓ ⇓ ⇓ - 5 RCVS is not a single disease entity but should be considered a common presentation of multiple disorders characterized by reversible vasoconstriction of the cerebral vasculature. (
  • 1 , 2 , 6 , 12 ⇓ - 14 Furthermore, a key feature of RCVS, segmental arterial vasoconstriction, may be absent early in the course of the disease. (
  • In the second part, we will review the imaging features of RCVS, including more recent work exploring associated imaging changes in the cerebral arterial vasculature beyond segmental vasoconstriction. (
  • In isolated blood-perfused rat lungs, brief periods of ventilation hypoxia (2% O 2 ) produce pulmonary vasoconstriction. (
  • The addition of angiotensin II (12-120 nM) to the perfusate during hypoxia resulted in marked pulmonary vasoconstriction in proportion to the amount of angiotensin II added (a maximal response to hypoxia occurred with 120 nM angiotensin II). (
  • 5. Small doses of almitrine enhanced the action of mild to moderate hypoxia, medium doses attenuated moderately severe hypoxia, whereas high doses depressed vasoconstriction due to all degrees of hypoxia. (
  • Hypoxia-induced Pulmonary Vasoconstriction (HPV) is an essential physiological process which ensures proper ventilationperfusion matching in pulmonary circulation with the ultimate aim of optimizing systemic oxygen delivery. (
  • Paddenberg R., Goldenberg A., Faulhammer P., Braun-Dullaeus R.C., Kummer W. (2003) Mitochondrial Complex II is Essential for Hypoxia-induced ROS Generation and Vasoconstriction in the Pulmonary Vasculature. (
  • Would chronically high catecholamines inducing vasoconstriction result in reduced Cerebral Blood Flow and Hypoxia? (
  • To compare the clinical, laboratory, and imaging features of patients with reversible cerebral vasoconstriction syndromes evaluated at 2 academic centers, compare subgroups, and investigate treatment effects. (
  • One hundred thirty-nine patients with reversible cerebral vasoconstriction syndromes. (
  • Patients with reversible cerebral vasoconstriction syndromes have a unique set of clinical imaging features, with no significant differences between subgroups. (
  • Under physiological circumstances, perivascular adipose cells (PVAT) attenuates agonist\induced vasoconstriction by releasing vasoactive substances including hydrogen peroxide, angiotensin 1C7, adiponectin, methyl palmitate, hydrogen sulfide, Zero and leptin. (
  • In this study we have examined the subcellar pathways along which angiotensin II (ANG II) causes renal vasoconstriction. (
  • Aminoamide local anesthetics induce vasoconstriction in vivo and in vitro . (
  • Aminoamide local anesthetics induce vasoconstriction at low doses and vasodilation at high doses [ 1 ]. (
  • These data describe a unique mechanism by which ANG II inhibits arterial myocyte BK currents, by reducing surface channel number, to induce vasoconstriction. (
  • Endothelium-dependent arterial vasoconstriction after balloon angioplasty. (
  • To determine whether balloon angioplasty can provoke arterial vasoconstriction independent of platelet aggregation and neurogenic input, we studied the spontaneous vasomotor effects of balloon dilatation in isolated, perfused whole-vessel segments of rabbit aorta and pig carotid artery. (
  • Significant arterial vasoconstriction was observed in the balloon angioplasty segments after dilatation with 5-mm balloons but not with 4-mm balloons. (
  • These findings demonstrate that stretch-pressure-induced arterial vasoconstriction may occur after balloon angioplasty, independent of platelet aggregation and neurogenic input. (
  • Finally, Arterial Spin Labeling (ASL) MRI can be used to non-invasively quantify perfusion of brain tissue, providing a measure of the impact of upstream arterial vasoconstriction on local cortical regions. (
  • Cutaneous vasoconstriction will occur because of the body's exposure to the severe cold. (
  • Nonnoradrenergic mechanism of reflex cutaneous vasoconstriction in men. (
  • We tested for a nonnoradrenergic mechanism of reflex cutaneous vasoconstriction with whole body progressive cooling in seven men. (
  • Thus, sympathetically mediated cutaneous vasoconstriction is one mechanism whereby MDMA causes hyperthermia. (
  • Reversal of cutaneous vasoconstriction by appropriate pharmacological means could be of therapeutic benefit in humans suffering from life-threatening hyperthermia induced by MDMA. (
  • Reversible cerebral vasoconstriction syndromes: analysis of 139 cases. (
  • Narrative review: reversible cerebral vasoconstriction syndromes. (
  • Naloxone (NX) potentiated epinephrine (EPI) induced submaximal vasoconstriction in canine renal and skeletal muscle arterial segments, yet had no vasoconstrictor action alone. (
  • Using the isolated perfused rat kidney model, we found that renal vasoconstriction produced by ANG II (100 pM) was not altered by the calmodulin antagonists calmidazolium (1 microM) and N-(6-aminohexyl)-5-chloro-1-naphthalensulfonamide (W-7, 10 microM) but was blunted by staurosporine (100 nM) and 1-(5-isoquinolinylsulfonyl)-2-methyl-piperazine (H-7, 50 microM), two structurally distinct putative protein kinase C inhibitors. (
  • The phorbol ester 4 alpha-phorbol 12,13-didecanoate (1-100 nM) did not alter renal vascular resistance, whereas phorbol 12-myristate 13-acetate (PMA, 1-100 nM) caused potent and dose-dependent vasoconstriction that was prevented by staurosporine (100 nM) and H-7 (50 microM). (
  • Mild atherosclerosis and hypercholesterolemia impair endothelium-mediated vasodilation in coronary arteries, and animal studies suggest that endothelial dysfunction predisposes a person to vasoconstriction and arterial spasm. (
  • We conclude that the intranasal administration of cocaine near the dose used for topical anesthesia causes vasoconstriction of the coronary arteries, with a decrease in the coronary blood flow, despite an increase in myocardial oxygen demand, and that these effects are mediated by alpha-adrenergic stimulation. (
  • 2,11-14 It has been suggested that the relative contribution of each receptor to endothelin-mediated vasoconstriction is different in canine conduit and resistance coronary arteries, in similarity with noncoronary arteries. (
  • Paradoxical vasoconstriction of stenotic coronary arteries has been reported during dynamic exercise and may be due to several factors such as alpha-adrenergic drive, a decreased release of nitric oxide, platelet aggregation with release of serotonin, or a passive collapse of the vessel wall. (
  • Exercise-induced vasoconstriction of stenotic coronary arteries is prevented by intracoronary administration of phentolamine. (
  • Stenotic coronary arteries have shown paradoxical vasoconstriction during isometric (4) but also dynamic exercise (5) . (
  • Medications that cause vasoconstriction include: antihistamines, decongestants, and stimulants. (
  • The extent of vasoconstriction may be slight or severe depending on the substance or circumstance. (
  • Severe vasoconstriction may result in symptoms of intermittent claudication . (
  • Vasoconstriction may be slight or severe. (
  • The initial CT angiography performed in the emergency room showed severe multisegmental vasoconstriction in the anterior and posterior circulation. (
  • Vasoconstriction is the narrowing of the blood vessels resulting from contraction of the muscular wall of the vessels, in particular the large arteries and small arterioles . (
  • blood pressure in mammals through vasoconstriction (i.e., contraction of blood vessels), this action requires a high concentration of hormone and is probably not a normal physiological effect. (
  • cutaneous blood vessels narrow (vasoconstriction), hairs fluff out to enhance thermal insulation, and appropriate warm-seeking behaviours are stimulated. (
  • Vasoconstriction is the narrowing (constriction) of blood vessels by small muscles in their walls. (
  • Understanding the vasoconstriction pathways activated by electrical stimuli will help create safe and effective devices for electrical control of blood vessels. (
  • We investigated the action of heparin in reducing the degree of vasoconstriction in the experimantal subarachnoid hemorrhage (SAH) models of rabbits. (
  • We found that chronic GPER deficiency is associated with increased endothelial prostanoid-mediated vasoconstriction but has no effect on endothelial nitric oxide bioactivity, gene expression of endothelial nitric oxide synthase and thromboxane prostanoid (TP) receptor, or vascular structure. (
  • 20 - 26 Furthermore, inhibitory effects of 17β-estradiol on COX-dependent responses to vasoconstrictors have suggested a role of estrogen receptors, 27 although the specific estrogen receptor(s) involved in endothelium-dependent vasoconstriction have not been identified. (
  • By this second component of the mechanism, the same stimulus directly acts on the carbonic anhydrase I isozyme (that might be functionally coupled with adrenergic receptors), so that its activation ensures an adequate pH for stimulus-receptor coupling for signal transduction into the cell, resulting in vasoconstriction. (
  • A variety of sigma receptor ligands, steroids and steroid metabolites were tested for the ability to augment EPI vasoconstrictions. (
  • Recent studies from this laboratory have indicated that sympathetic α-receptor-mediated coronary vasoconstriction can compete with local metabolic vasodilation to reduce the oxygen supply to the myocardium. (
  • In this study we used anesthetized, open-chest dogs to test the hypothesis that α-receptor-mediated vasoconstriction occurs predominantly in epicardial vessels, which are partially removed from the metabolic milieu in the myocardium. (
  • These data suggest that, contrary to the proposed hypothesis, adrenergic a-receptor-mediated vasoconstriction in the large coronary vessels is not proportionally greater than that observed in the total coronary vascular bed. (
  • These studies demonstrate that experimental hypercholesterolemia is characterized by enhanced coronary vasoconstriction to endothelins in vitro, the mechanism of which is mediated mainly through the ETB receptor. (
  • 7-10 The relative contribution made by each receptor to endothelin-mediated vasoconstriction is different between the two vessel types. (
  • Paired with the observed maintenance KCl-mediated constriction, it appears an acute bout of exercise is able to attenuate α-adrenergic receptor-mediated vasoconstriction in the femoral artery. (
  • Listed below are some combinations of symptoms associated with Peripheral vasoconstriction, as listed in our database. (
  • A classical view of sympathetic vasoconstriction describes the release of norepinephrine (NE) which binds postsynaptic α-adrenergic receptors. (
  • Medications may be used to treat vasoconstriction or to cause vasoconstriction. (
  • Can sodium channel blockers treat vasoconstriction and ED? (
  • Because the effects of NE were blocked at sites showing significant reflex vasoconstriction, a nonnoradrenergic mechanism in human skin is indicated, probably via a sympathetic cotransmitter. (
  • Local heating (40 degrees C) was achieved with a Peltier element, and reflex vasoconstriction induced by immersion of the contra-lateral hand and forearm for 3 min in water at 15 degrees C. The change in skin blood flow was measured and a vasoconstriction index (VAC: cooling/before cooling) calculated. (
  • Levobupivacaine, ropivacaine, mepivacaine, and lidocaine produce vasoconstriction both in vivo and in vitro [ 1 , 5 - 12 ]. (
  • There are two distinct populations of α-adrenergic receptors (α 1 and α 2 ) found of vascular smooth muscle, both of which produce vasoconstriction when stimulated. (
  • Regression analyses were performed to determine the relationship between the reported physicochemical properties of local anesthetics and the local anesthetic concentration that produced 50% (ED 50 ) of the local anesthetic-induced maximum vasoconstriction. (
  • On a larger level, vasoconstriction is one mechanism by which the body regulates and maintains mean arterial pressure . (
  • The mechanism that leads to vasoconstriction results from the increased concentration of calcium (Ca 2+ ions ) within vascular smooth muscle cells . (
  • In the present investigation we studied the relationship between alpha- and beta-adrenergic agonists and CA activity in vasoconstriction mechanism. (
  • Our findings suggest that increased TMEM16A expression and activity comprise an important pathologic mechanism underlying the vasoconstriction and remodelling of pulmonary arteries in PAH. (
  • The exact mechanism that is responsible for the reported stenosis vasoconstriction is not clear but may involve several factors such as an enhanced sympathetic stimulation during exercise, endothelial dysfunction with reduced nitric oxide (NO) release or production, increased platelet aggregation with release of serotonin and thromboxane A2, or a passive collapse of the stenotic vessel segment within the stenosis due to the increase in flow velocity during exercise (Venturi effect). (
  • Neural inhibitors significantly reduced low-voltage arterial constriction, but did not affect high-voltage arterial or venous constriction, indicating that high-voltage stimuli activate non-neural vasoconstriction pathways. (
  • We demonstrate that low-voltage stimuli induce reversible vasoconstriction through neural pathways, while high-voltage stimuli activate non-neural pathways, likely in addition to neural stimulation. (
  • This finding suggests that exercise-induced vasoconstriction is mediated not only by endothelial dysfunction but also by alpha-adrenergic mechanisms. (
  • Two neuroradiologists reviewed the final cerebral angiographic finding of carotid artery stent placement to evaluate the presence of vasoconstriction or vasodilation. (
  • Although coronary vasoconstriction existed in stenotic vessel segments in control patients, phentolamine-treated patients showed exercise-induced vasodilation without difference in patients with and without chronic beta-blockade. (
  • Additional experiments were carried out in rabbit aortas to determine the roles of the endothelium, extracellular calcium, indomethacin, ibuprofen, and calcium-channel blockade in modulating angioplasty-induced vasoconstriction. (
  • The vasoconstriction was only partially inhibited by calcium channel blockade with verapamil. (
  • Alphaadrenergic blockade with phentolamine completely eliminated EPI plus NX induced vasoconstriction. (
  • 2. In the absence of NO blockade, the AT1-R antagonist L-158809 (500 nM) antagonized the Ang II-induced vasoconstrictions, while the AT2-R antagonist PD-123319 (500 nM) had no effect. (
  • 6. Similar to PD-123319, during NO blockade the AT2-R antagonist CGP-42112A at 5 nM decreased by 50% the 0.1 nM Ang II-induced vasoconstriction and at 500 nM had no effect on 10 nM Ang II-induced vasoconstriction. (
  • Heterogeneous microvascular coronary alpha-adrenergic vasoconstriction. (
  • The decrease in maximum α-adrenergic vasoconstriction may be attributed to vascular RAS. (
  • Similar postangioplasty vasoconstriction was observed in the pig carotid arteries (decrease in minimal vessel cross-sectional area of 41% [angioplasty segment] versus 2% [control segment]) (p less than 0.005). (
  • Does the vasoconstriction decrease blood vessel volume at the same time? (
  • Arterial smooth muscle cell (myocyte) BK channels serve as a negative regulator of pressure-induced vasoconstriction (the myogenic response) and are modulated by multiple vasoconstrictor and vasodilator agonists and stimuli ( 11 , 24 , 31 - 33 ). (
  • In patients with dysfunctional endothelium, serotonin causes intense vasoconstriction because of its unopposed effects on vascular smooth muscle. (
  • Cerebral vasoconstriction cases after carotid endarterectomy have often been reported. (
  • the mean time of diagnosis of intracranial hemorrhage was 2.2 days from headache onset and the mean time to diagnosis of vasoconstriction was 6.6 days. (
  • 4 Endothelin binding to vascular smooth muscle ETA and ETB receptors mediates vasoconstriction, whereas ETB receptors on the vascular endothelium mediate a vasodilator response, presumably through increased production and release of nitric oxide and/or prostacyclin 6 and activation of potassium channels. (
  • To determine whether epinephrine facilitates neurogenic vasoconstriction in humans, we contrasted forearm vasoconstrictor responses to a reflex stimulus (lower body negative pressure [LBNP]) and to intraarterial NE before, during, and 30 min after infusion of epinephrine (50 ng/min) or isoproterenol (10 or 25 ng/min) into a brachial artery. (
  • Impairment of sympathetic pulmonary vasoconstriction by 3-methylindole in cattle. (
  • These studies provide convincing evidence that the same sympathetic stimulation in resting skeletal muscle produces more vasoconstriction than in exercising skeletal muscle. (
  • The aim of this study was to quantify the reflex sympathetic vasoconstriction in skin at different depths. (
  • We conclude that sympathetic skin vasoconstriction does not significantly differ in two compartments, as probed with fibres separated by 0.25 and 0.14 mm. (
  • Epinephrine facilitates neurogenic vasoconstriction in humans. (
  • These experiments provide the first hemodynamic evidence in humans that epinephrine and isoproterenol facilitate neurogenic vasoconstriction. (
  • To define the temporal characteristics of cocaine-induced coronary vasoconstriction in humans and to assess the relation between cocaine-induced coronary vasoconstriction and the blood concentration of cocaine and its main metabolites. (
  • Intranasal cocaine causes recurrent coronary vasoconstriction, which may be due to its metabolites. (
  • We report a 55-year-old woman with recurrent cerebral vasoconstriction postoperatively. (
  • The potency of the vasoconstriction in the endothelium-denuded aorta induced by local anesthetics is determined primarily by lipid solubility and, in part, by other physicochemical properties including potency and pKa. (
  • 3. Perfusing kidneys in the presence of either NO synthase inhibitors, L-NAME (100 microM) or L-NOARG (1 mM), or soluble guanylyl cyclase inhibitor, LY-83583 (10 microM), significantly increased both molar pD2 (from 9.40+/-0.25 to 10.36+/-0.11) and Emax values (from 24.9+/-3.1 to 79.9+/-4.9 mmHg) of the concentration-response curve for Ang II-induced vasoconstriction. (
  • Models of aging have shown that this is due, in part, to increased prostaglandin H synthase (PGHS)-dependent vasoconstriction. (
  • Factors that trigger vasoconstriction can be exogenous or endogenous in origin. (
  • Generalized vasoconstriction usually results in an increase in systemic blood pressure, but it may also occur in specific tissues, causing a localized reduction in blood flow. (
  • Cerebral vasoconstriction may occur after carotid artery stenting more frequently than expected. (
  • Conclusions- This study reveals for the first time that apart from rapidly desensitizing homomeric P2X1Rs, heteromeric P2X1/4Rs contribute to the sustained component of the purinergic-mediated vasoconstriction in RMCA. (
  • This study investigated whether KMUP-1 reduces pulmonary vasoconstriction in isolated pulmonary arteries (PAs) and attenuates 5-HT-inhibited K + channel activities in PASMCs. (
  • Indirect inhibitors (usually act by increasing PA pressures, which overcome vasoconstriction) include vasopressors, volume overload, mitral stenosis, and thromboembolism. (
  • What is the role of endothelial cells in cocaine-induced vasoconstriction? (
  • Vasoconstriction is constriction or narrowing of a blood vessel. (