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NatriuresisDiuresisSodiumKidneyAtrial Natriuretic FactorRenal CirculationNatriuretic AgentsGlomerular Filtration RateBlood PressureFurosemideWater-Electrolyte BalanceAldosteroneAminohippuric AcidsDiureticsInulinKidney TubulesReninKidney MedullaAngiotensin II Type 2 Receptor BlockersSodium, DietaryAngiotensin IIIElectrolytesBendroflumethiazideKidney Tubules, ProximalBlood VolumeBufanolidesSodium ChloridePotassiumSodium Chloride, DietaryUrinationDenervationHypertensionVasopressinsUrineFenoldopamArginine VasopressinReceptor, Angiotensin, Type 2DogsSodium Chloride SymportersIsotonic SolutionsCyclic GMPRenin-Angiotensin SystemOsmolar ConcentrationFludrocortisoneUrodynamicsSaline Solution, HypertonicHyponatremiaSolute Carrier Family 12, Member 1Kallikrein-Kinin SystemKidney Tubules, DistalNephronsHemodynamicsNatriuretic PeptidesAngiotensin IIDehydrationReceptors, Atrial Natriuretic FactorRats, Sprague-DawleyKidney CortexKidney Function TestsLithiumDiet, Sodium-RestrictedHydrostatic PressureWater DeprivationSodium Chloride Symporter InhibitorsParabiosisRenal AgentsMeclofenamic AcidPuncturesThiorphanPolyuriaPlasma SubstitutesHypertension, RenalMelanocyte-Stimulating HormonesWater-Electrolyte ImbalanceSodium-Potassium-Exchanging ATPaseRenal ArteryAnesthesiaChlorothiazideNeprilysinOxytocinImidazolesMetoclopramideRegional Blood FlowPlasma VolumeRats, WistarKidney Tubules, CollectingPyridinesRats, Inbred SHRTetrazolesImmersionReceptors, Dopamine D1DihydroxyphenylalanineAngiotensin II Type 1 Receptor BlockersBenzimidazolesRats, Inbred StrainsDrinkingLoop of HenleCardenolidesMetolazoneExtracellular SpaceHematocritDopamineNG-Nitroarginine Methyl EsterEpithelial Sodium ChannelsRats, Inbred WKYSodium-Potassium-Chloride SymportersSodium-Phosphate Cotransporter Proteins, Type IIHypernatremiaReceptors, VasopressinNephrectomyDose-Response Relationship, DrugInjections, IntraventricularCreatinineSodium-Hydrogen AntiporterInappropriate ADH SyndromeImidazoline ReceptorsKidney Concentrating AbilityPerfusionp-Aminohippuric AcidInfusions, IntravenousDesoxycorticosteroneAntihypertensive AgentsDeamino Arginine VasopressinKininsPressureNitric OxideChloridesWaterAngiotensin-Converting Enzyme InhibitorsBenzazepinesRats, Mutant Strains2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepineKidney Pelvis
Natriuresis: Sodium excretion by URINATION.Diuresis: An increase in the excretion of URINE. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)Sodium: A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Atrial Natriuretic Factor: A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight PEPTIDES derived from a common precursor and secreted mainly by the HEART ATRIUM. All these peptides share a sequence of about 20 AMINO ACIDS.Renal Circulation: The circulation of the BLOOD through the vessels of the KIDNEY.Natriuretic Agents: Endogenous or exogenous chemicals that regulate the WATER-ELECTROLYTE BALANCE in the body. They consist of peptides and non-peptide compounds.Glomerular Filtration Rate: The volume of water filtered out of plasma through glomerular capillary walls into Bowman's capsules per unit of time. It is considered to be equivalent to INULIN clearance.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Furosemide: A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.Water-Electrolyte Balance: The balance of fluid in the BODY FLUID COMPARTMENTS; total BODY WATER; BLOOD VOLUME; EXTRACELLULAR SPACE; INTRACELLULAR SPACE, maintained by processes in the body that regulate the intake and excretion of WATER and ELECTROLYTES, particularly SODIUM and POTASSIUM.Aldosterone: A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.Aminohippuric Acids: A group of glycine amides of aminobenzoic acids.Diuretics: Agents that promote the excretion of urine through their effects on kidney function.Inulin: A starch found in the tubers and roots of many plants. Since it is hydrolyzable to FRUCTOSE, it is classified as a fructosan. It has been used in physiologic investigation for determination of the rate of glomerular function.Kidney Tubules: Long convoluted tubules in the nephrons. They collect filtrate from blood passing through the KIDNEY GLOMERULUS and process this filtrate into URINE. Each renal tubule consists of a BOWMAN CAPSULE; PROXIMAL KIDNEY TUBULE; LOOP OF HENLE; DISTAL KIDNEY TUBULE; and KIDNEY COLLECTING DUCT leading to the central cavity of the kidney (KIDNEY PELVIS) that connects to the URETER.Renin: A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19.Kidney Medulla: The internal portion of the kidney, consisting of striated conical masses, the renal pyramids, whose bases are adjacent to the cortex and whose apices form prominent papillae projecting into the lumen of the minor calyces.Angiotensin II Type 2 Receptor Blockers: Agents that antagonize the ANGIOTENSIN II TYPE 2 RECEPTOR.Sodium, Dietary: Sodium or sodium compounds used in foods or as a food. The most frequently used compounds are sodium chloride or sodium glutamate.Angiotensin III: A heptapeptide formed from ANGIOTENSIN II after the removal of an amino acid at the N-terminal by AMINOPEPTIDASE A. Angiotensin III has the same efficacy as ANGIOTENSIN II in promoting ALDOSTERONE secretion and modifying renal blood flow, but less vasopressor activity (about 40%).Electrolytes: Substances that dissociate into two or more ions, to some extent, in water. Solutions of electrolytes thus conduct an electric current and can be decomposed by it (ELECTROLYSIS). (Grant & Hackh's Chemical Dictionary, 5th ed)Bendroflumethiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. It has been used in the treatment of familial hyperkalemia, hypertension, edema, and urinary tract disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p810)Kidney Tubules, Proximal: The renal tubule portion that extends from the BOWMAN CAPSULE in the KIDNEY CORTEX into the KIDNEY MEDULLA. The proximal tubule consists of a convoluted proximal segment in the cortex, and a distal straight segment descending into the medulla where it forms the U-shaped LOOP OF HENLE.Blood Volume: Volume of circulating BLOOD. It is the sum of the PLASMA VOLUME and ERYTHROCYTE VOLUME.Bufanolides: Cyclopentanophenanthrenes with a 6-membered lactone ring attached at the 17-position and SUGARS attached at the 3-position. They are found in BUFONIDAE and often possess cardiotonic properties.Sodium Chloride: A ubiquitous sodium salt that is commonly used to season food.Potassium: An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.Sodium Chloride, Dietary: Sodium chloride used in foods.Urination: Discharge of URINE, liquid waste processed by the KIDNEY, from the body.Denervation: The resection or removal of the nerve to an organ or part. (Dorland, 28th ed)Hypertension: 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.Vasopressins: 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.Urine: Liquid by-product of excretion produced in the kidneys, temporarily stored in the bladder until discharge through the URETHRA.Fenoldopam: A dopamine D1 receptor agonist that is used as an antihypertensive agent. It lowers blood pressure through arteriolar vasodilation.Arginine Vasopressin: 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.Receptor, Angiotensin, Type 2: An angiotensin receptor subtype that is expressed at high levels in fetal tissues. Many effects of the angiotensin type 2 receptor such as VASODILATION and sodium loss are the opposite of that of the ANGIOTENSIN TYPE 1 RECEPTOR.Dogs: 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)Sodium Chloride Symporters: A subclass of symporters found in KIDNEY TUBULES, DISTAL that are the major pathway for salt resorption. Inhibition of these symporters by BENZOTHIADIAZINES is the basis of action of some DIURETICS.Isotonic Solutions: Solutions having the same osmotic pressure as blood serum, or another solution with which they are compared. (From Grant & Hackh's Chemical Dictionary, 5th ed & Dorland, 28th ed)Cyclic GMP: Guanosine cyclic 3',5'-(hydrogen phosphate). A guanine nucleotide containing one phosphate group which is esterified to the sugar moiety in both the 3'- and 5'-positions. It is a cellular regulatory agent and has been described as a second messenger. Its levels increase in response to a variety of hormones, including acetylcholine, insulin, and oxytocin and it has been found to activate specific protein kinases. (From Merck Index, 11th ed)Renin-Angiotensin System: A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM.Osmolar Concentration: The concentration of osmotically active particles in solution expressed in terms of osmoles of solute per liter of solution. Osmolality is expressed in terms of osmoles of solute per kilogram of solvent.Fludrocortisone: A synthetic mineralocorticoid with anti-inflammatory activity.Urodynamics: The mechanical laws of fluid dynamics as they apply to urine transport.Saline Solution, Hypertonic: Hypertonic sodium chloride solution. A solution having an osmotic pressure greater than that of physiologic salt solution (0.9 g NaCl in 100 ml purified water).Hyponatremia: Deficiency of sodium in the blood; salt depletion. (Dorland, 27th ed)Solute Carrier Family 12, Member 1: Na-K-Cl transporter in the ASCENDING LIMB OF LOOP OF HENLE. It mediates active reabsorption of sodium chloride and is inhibited by LOOP DIURETICS such as FUROSEMIDE; and BUMETANIDE. Mutations in the gene encoding SLC12A1 are associated with a BARTTER SYNDROME.Kallikrein-Kinin System: A system of metabolic interactions by products produced in the distal nephron of the KIDNEY. These products include KALLIKREIN; KININS; KININASE I; KININASE II; and ENKEPHALINASE. This system participates in the control of renal functions. It interacts with the RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM to regulate BLOOD PRESSURE, generation of PROSTAGLANDINS, release of VASOPRESSINS, and WATER-ELECTROLYTE BALANCE.Kidney Tubules, Distal: The portion of renal tubule that begins from the enlarged segment of the ascending limb of the LOOP OF HENLE. It reenters the KIDNEY CORTEX and forms the convoluted segments of the distal tubule.Nephrons: The functional units of the kidney, consisting of the glomerulus and the attached tubule.Hemodynamics: The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.Natriuretic Peptides: Peptides that regulate the WATER-ELECTROLYTE BALANCE in the body, also known as natriuretic peptide hormones. Several have been sequenced (ATRIAL NATRIURETIC FACTOR; BRAIN NATRIURETIC PEPTIDE; C-TYPE NATRIURETIC PEPTIDE).Angiotensin II: 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.Dehydration: The condition that results from excessive loss of water from a living organism.Receptors, Atrial Natriuretic Factor: Cell surface proteins that bind ATRIAL NATRIURETIC FACTOR with high affinity and trigger intracellular changes influencing the behavior of cells. They contain intrinsic guanylyl cyclase activity.Rats, Sprague-Dawley: 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.Kidney Cortex: The outer zone of the KIDNEY, beneath the capsule, consisting of KIDNEY GLOMERULUS; KIDNEY TUBULES, DISTAL; and KIDNEY TUBULES, PROXIMAL.Kidney Function Tests: Laboratory tests used to evaluate how well the kidneys are working through examination of blood and urine.Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight [6.938; 6.997]. Salts of lithium are used in treating BIPOLAR DISORDER.Diet, Sodium-Restricted: A diet which contains very little sodium chloride. It is prescribed by some for hypertension and for edematous states. (Dorland, 27th ed)Hydrostatic Pressure: The pressure due to the weight of fluid.Water Deprivation: The withholding of water in a structured experimental situation.Sodium Chloride Symporter Inhibitors: Agents that inhibit SODIUM CHLORIDE SYMPORTERS. They act as DIURETICS. Excess use is associated with HYPOKALEMIA.Parabiosis: The experimental joining of two individuals for the purpose of studying the effects of one on the other.Renal Agents: Drugs used for their effects on the kidneys' regulation of body fluid composition and volume. The most commonly used are the diuretics. Also included are drugs used for their antidiuretic and uricosuric actions, for their effects on the kidneys' clearance of other drugs, and for diagnosis of renal function.Meclofenamic Acid: A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis.Punctures: Incision of tissues for injection of medication or for other diagnostic or therapeutic procedures. Punctures of the skin, for example may be used for diagnostic drainage; of blood vessels for diagnostic imaging procedures.Thiorphan: A potent inhibitor of membrane metalloendopeptidase (ENKEPHALINASE). Thiorphan potentiates morphine-induced ANALGESIA and attenuates naloxone-precipitated withdrawal symptoms.Polyuria: Urination of a large volume of urine with an increase in urinary frequency, commonly seen in diabetes (DIABETES MELLITUS; DIABETES INSIPIDUS).Plasma Substitutes: Any liquid used to replace blood plasma, usually a saline solution, often with serum albumins, dextrans or other preparations. These substances do not enhance the oxygen- carrying capacity of blood, but merely replace the volume. They are also used to treat dehydration.Hypertension, Renal: Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.Melanocyte-Stimulating Hormones: Peptides with the ability to stimulate pigmented cells MELANOCYTES in mammals and MELANOPHORES in lower vertebrates. By stimulating the synthesis and distribution of MELANIN in these pigmented cells, they increase coloration of skin and other tissue. MSHs, derived from pro-opiomelanocortin (POMC), are produced by MELANOTROPHS in the INTERMEDIATE LOBE OF PITUITARY; CORTICOTROPHS in the ANTERIOR LOBE OF PITUITARY, and the hypothalamic neurons in the ARCUATE NUCLEUS OF HYPOTHALAMUS.Water-Electrolyte Imbalance: Disturbances in the body's WATER-ELECTROLYTE BALANCE.Sodium-Potassium-Exchanging ATPase: An enzyme that catalyzes the active transport system of sodium and potassium ions across the cell wall. Sodium and potassium ions are closely coupled with membrane ATPase which undergoes phosphorylation and dephosphorylation, thereby providing energy for transport of these ions against concentration gradients.Renal Artery: A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters.Anesthesia: 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.Chlorothiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p812)Neprilysin: Enzyme that is a major constituent of kidney brush-border membranes and is also present to a lesser degree in the brain and other tissues. It preferentially catalyzes cleavage at the amino group of hydrophobic residues of the B-chain of insulin as well as opioid peptides and other biologically active peptides. The enzyme is inhibited primarily by EDTA, phosphoramidon, and thiorphan and is reactivated by zinc. Neprilysin is identical to common acute lymphoblastic leukemia antigen (CALLA Antigen), an important marker in the diagnosis of human acute lymphocytic leukemia. There is no relationship with CALLA PLANT.Oxytocin: A nonapeptide hormone released from the neurohypophysis (PITUITARY GLAND, POSTERIOR). It differs from VASOPRESSIN by two amino acids at residues 3 and 8. Oxytocin acts on SMOOTH MUSCLE CELLS, such as causing UTERINE CONTRACTIONS and MILK EJECTION.Imidazoles: 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).Metoclopramide: A dopamine D2 antagonist that is used as an antiemetic.Regional Blood Flow: The flow of BLOOD through or around an organ or region of the body.Plasma Volume: Volume of PLASMA in the circulation. It is usually measured by INDICATOR DILUTION TECHNIQUES.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Kidney Tubules, Collecting: Straight tubes commencing in the radiate part of the kidney cortex where they receive the curved ends of the distal convoluted tubules. In the medulla the collecting tubules of each pyramid converge to join a central tube (duct of Bellini) which opens on the summit of the papilla.Pyridines: Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.Rats, Inbred SHR: A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.TetrazolesImmersion: The placing of a body or a part thereof into a liquid.Receptors, Dopamine D1: A subfamily of G-PROTEIN-COUPLED RECEPTORS that bind the neurotransmitter DOPAMINE and modulate its effects. D1-class receptor genes lack INTRONS, and the receptors stimulate ADENYLYL CYCLASES.Dihydroxyphenylalanine: A beta-hydroxylated derivative of phenylalanine. The D-form of dihydroxyphenylalanine has less physiologic activity than the L-form and is commonly used experimentally to determine whether the pharmacological effects of LEVODOPA are stereospecific.Angiotensin II Type 1 Receptor Blockers: Agents that antagonize ANGIOTENSIN II TYPE 1 RECEPTOR. Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN. Some are used as ANTIHYPERTENSIVE AGENTS.Benzimidazoles: Compounds with a BENZENE fused to IMIDAZOLES.Rats, Inbred Strains: 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.Drinking: The consumption of liquids.Loop of Henle: The U-shaped portion of the renal tubule in the KIDNEY MEDULLA, consisting of a descending limb and an ascending limb. It is situated between the PROXIMAL KIDNEY TUBULE and the DISTAL KIDNEY TUBULE.Cardenolides: C(23)-steroids with methyl groups at C-10 and C-13 and a five-membered lactone at C-17. They are aglycone constituents of CARDIAC GLYCOSIDES and must have at least one double bond in the molecule. The class includes cardadienolides and cardatrienolides. Members include DIGITOXIN and DIGOXIN and their derivatives and the STROPHANTHINS.Metolazone: A quinazoline-sulfonamide derived DIURETIC that functions by inhibiting SODIUM CHLORIDE SYMPORTERS.Extracellular Space: Interstitial space between cells, occupied by INTERSTITIAL FLUID as well as amorphous and fibrous substances. For organisms with a CELL WALL, the extracellular space includes everything outside of the CELL MEMBRANE including the PERIPLASM and the cell wall.Hematocrit: The volume of packed RED BLOOD CELLS in a blood specimen. The volume is measured by centrifugation in a tube with graduated markings, or with automated blood cell counters. It is an indicator of erythrocyte status in disease. For example, ANEMIA shows a low value; POLYCYTHEMIA, a high value.Dopamine: One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.NG-Nitroarginine Methyl Ester: A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.Epithelial Sodium Channels: Sodium channels found on salt-reabsorbing EPITHELIAL CELLS that line the distal NEPHRON; the distal COLON; SALIVARY DUCTS; SWEAT GLANDS; and the LUNG. They are AMILORIDE-sensitive and play a critical role in the control of sodium balance, BLOOD VOLUME, and BLOOD PRESSURE.Rats, Inbred WKY: A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).Sodium-Potassium-Chloride Symporters: A subclass of symporters that specifically transport SODIUM CHLORIDE and/or POTASSIUM CHLORIDE across cellular membranes in a tightly coupled process.Sodium-Phosphate Cotransporter Proteins, Type II: A family of sodium-phosphate cotransporter proteins with eight transmembrane domains. They are present primarily in the KIDNEY and SMALL INTESTINE and are responsible for renal and small intestinal epithelial transport of phosphate.Hypernatremia: Excessive amount of sodium in the blood. (Dorland, 27th ed)Receptors, Vasopressin: Specific molecular sites or proteins on or in cells to which VASOPRESSINS bind or interact in order to modify the function of the cells. Two types of vasopressin receptor exist, the V1 receptor in the vascular smooth muscle and the V2 receptor in the kidneys. The V1 receptor can be subdivided into V1a and V1b (formerly V3) receptors.Nephrectomy: Excision of kidney.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Injections, Intraventricular: Injections into the cerebral ventricles.CreatinineSodium-Hydrogen Antiporter: A plasma membrane exchange glycoprotein transporter that functions in intracellular pH regulation, cell volume regulation, and cellular response to many different hormones and mitogens.Inappropriate ADH Syndrome: A condition of HYPONATREMIA and renal salt loss attributed to overexpansion of BODY FLUIDS resulting from sustained release of ANTIDIURETIC HORMONES which stimulates renal resorption of water. It is characterized by normal KIDNEY function, high urine OSMOLALITY, low serum osmolality, and neurological dysfunction. Etiologies include ADH-producing neoplasms, injuries or diseases involving the HYPOTHALAMUS, the PITUITARY GLAND, and the LUNG. This syndrome can also be drug-induced.Imidazoline Receptors: Receptors of CLONIDINE and other IMIDAZOLINES. Activity of the ligands was earlier attributed to ADRENERGIC ALPHA-2 RECEPTORS. Endogenous ligands include AGMATINE, imidazoleacetic acid ribotide, and harman.Kidney Concentrating Ability: The ability of the kidney to excrete in the urine high concentrations of solutes from the blood plasma.Perfusion: Treatment process involving the injection of fluid into an organ or tissue.p-Aminohippuric Acid: The glycine amide of 4-aminobenzoic acid. Its sodium salt is used as a diagnostic aid to measure effective renal plasma flow (ERPF) and excretory capacity.Infusions, Intravenous: The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.Desoxycorticosterone: A steroid metabolite that is the 11-deoxy derivative of CORTICOSTERONE and the 21-hydroxy derivative of PROGESTERONE.Antihypertensive Agents: Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.Deamino Arginine Vasopressin: A synthetic analog of the pituitary hormone, ARGININE VASOPRESSIN. Its action is mediated by the VASOPRESSIN receptor V2. It has prolonged antidiuretic activity, but little pressor effects. It also modulates levels of circulating FACTOR VIII and VON WILLEBRAND FACTOR.Kinins: A generic term used to describe a group of polypeptides with related chemical structures and pharmacological properties that are widely distributed in nature. These peptides are AUTACOIDS that act locally to produce pain, vasodilatation, increased vascular permeability, and the synthesis of prostaglandins. Thus, they comprise a subset of the large number of mediators that contribute to the inflammatory response. (From Goodman and Gilman's The Pharmacologic Basis of Therapeutics, 8th ed, p588)Pressure: A type of stress exerted uniformly in all directions. Its measure is the force exerted per unit area. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)Nitric Oxide: 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.Chlorides: Inorganic compounds derived from hydrochloric acid that contain the Cl- ion.Water: A clear, odorless, tasteless liquid that is essential for most animal and plant life and is an excellent solvent for many substances. The chemical formula is hydrogen oxide (H2O). (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Angiotensin-Converting Enzyme Inhibitors: A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.Benzazepines: Compounds with BENZENE fused to AZEPINES.Rats, Mutant Strains: Rats bearing mutant genes which are phenotypically expressed in the animals.2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine: A selective D1 dopamine receptor agonist used primarily as a research tool.Kidney Pelvis: The flattened, funnel-shaped expansion connecting the URETER to the KIDNEY CALICES.

Immediate and early renal function after living donor transplantation. (1/1093)

BACKGROUND: In order to assess the immediate renal function after living donor transplantation, renal function was compared in eight renal allograft recipients and their living related kidney donors during the first 24 h after transplantation. METHODS: Substantial and comparable intraoperative volume loading with Ringer's acetate and mannitol was performed together with the administration of frusemide. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were estimated by the clearances of inulin and p-aminohippurane, respectively. Tubular reabsorptive function and injury were estimated from the clearance of lithium, the fractional excretion of sodium and the urinary excretion of N-acetyl-beta-glucosaminidase. RESULTS: One hour after completion of surgery, GFR (54 +/- 7 ml/min) and ERPF (294 +/- 35 ml/min) were only 30% lower in the grafts than in the remaining donor kidneys, increasing to similar levels within 3 h. Only minor tubular dysfunction and injury were revealed in the grafted kidneys, and these tended to normalize within 24 h. CONCLUSIONS: By the present transplantation procedure comprising short ischaemia time and substantial volume expansion combined with mannitol and frusemide administration, kidneys from living donors regain nearly normal function within a few hours after transplantation.  (+info)

Role of renal medullary adenosine in the control of blood flow and sodium excretion. (2/1093)

This study determined the levels of adenosine in the renal medullary interstitium using microdialysis and fluorescence HPLC techniques and examined the role of endogenous adenosine in the control of medullary blood flow and sodium excretion by infusing the specific adenosine receptor antagonists or agonists into the renal medulla of anesthetized Sprague-Dawley rats. Renal cortical and medullary blood flows were measured using laser-Doppler flowmetry. Analysis of microdialyzed samples showed that the adenosine concentration in the renal medullary interstitial dialysate averaged 212 +/- 5.2 nM, which was significantly higher than 55.6 +/- 5.3 nM in the renal cortex (n = 9). Renal medullary interstitial infusion of a selective A1 antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 300 pmol. kg-1. min-1, n = 8), did not alter renal blood flows, but increased urine flow by 37% and sodium excretion by 42%. In contrast, renal medullary infusion of the selective A2 receptor blocker 3, 7-dimethyl-1-propargylxanthine (DMPX; 150 pmol. kg-1. min-1, n = 9) decreased outer medullary blood flow (OMBF) by 28%, inner medullary blood flows (IMBF) by 21%, and sodium excretion by 35%. Renal medullary interstitial infusion of adenosine produced a dose-dependent increase in OMBF, IMBF, urine flow, and sodium excretion at doses from 3 to 300 pmol. kg-1. min-1 (n = 7). These effects of adenosine were markedly attenuated by the pretreatment of DMPX, but unaltered by DPCPX. Infusion of a selective A3 receptor agonist, N6-benzyl-5'-(N-ethylcarbonxamido)adenosine (300 pmol. kg-1. min-1, n = 6) into the renal medulla had no effect on medullary blood flows or renal function. Glomerular filtration rate and arterial pressure were not changed by medullary infusion of any drugs. Our results indicate that endogenous medullary adenosine at physiological concentrations serves to dilate medullary vessels via A2 receptors, resulting in a natriuretic response that overrides the tubular A1 receptor-mediated antinatriuretic effects.  (+info)

Hemodynamic and renal effects of U-46619, a TXA2/PGH2 analog, in late-pregnant rats. (3/1093)

The vasoconstrictor effects of pressor agents are attenuated during pregnancy. Thromboxane A2 (TXA2) is produced in great quantities during hypertension in pregnancy, and therefore it is important to know whether pregnancy modifies the pressor effects of TXA2. The TXA2 analog U-46619 was infused in anesthetized, acutely prepared and conscious, chronically prepared late-pregnant and nonpregnant female rats to examine its systemic hemodynamic and renal effects. Mean arterial pressure (MAP) and total peripheral resistance (TPR) were lower in anesthetized pregnant than nonpregnant rats (P < 0.01). The infusion of U-46619 into the aortic arch resulted in elevation of MAP only in pregnant rats, due to a greater elevation of TPR (60 +/- 17%) compared with nonpregnant rats (36 +/- 6%, P < 0.05). The pressor effect of intravenously infused U-46619 was also enhanced in conscious pregnant versus nonpregnant rats, and the increase in renal vascular resistance was undiminished. U-46619 increased hematocrit and plasma protein concentration more during pregnancy, which suggested greater reduction of plasma volume. The urinary excretion of sodium (-1.49 +/- 0.25 vs. -0.54 +/- 0.24 micromol/min) and water was reduced more in pregnant than nonpregnant rats during U-46619 (P < 0.01). Thus the MAP and renal effects of the TXA2 analog are exaggerated during pregnancy in the rat.  (+info)

The subtype 2 of angiotensin II receptors and pressure-natriuresis in adult rat kidneys. (4/1093)

The present work examined the effects of the subtype 2 of angiotensin II (AT2) receptors on the pressure-natriuresis using a new peptide agonist, and the possible involvement of cyclic guanosine 3', 5' monophosphate (cyclic GMP) in these effects. In adult anaesthetized rats (Inactin, 100 mg kg(-1), i.p.) deprived of endogenous angiotensin II by angiotensin converting enzyme inhibition (quinapril, 10 mg kg(-1), i.v.), T2-(Ang II 4-8)2 (TA), a highly specific AT2 receptor agonist (5, 10 and 30 microg kg(-1) min(-1), i.v.) or its solvent was infused in four groups. Renal functions were studied at renal perfusion pressures (RPP) of 90, 110 and 130 mmHg and urinary cyclic GMP excretion when RPP was at 130 mmHg. The effects of TA (10 microg kg(-1) min(-1)) were reassessed in animals pretreated with PD 123319 (PD, 50 microg kg(-1) min(-1), i.v.), an AT2 receptor antagonist and the action of the same dose of PD alone was also determined. Increases in RPP from 90 to 130 mmHg did not change renal blood flow (RBF) but induced 8 and 15 fold increases in urinary flow and sodium excretion respectively. The 5 microg kg(-1) min(-1) dose of TA was devoid of action. The 10 and 30 microg kg(-1) min(-1) doses did not alter total RBF and glomerular filtration rate, but blunted pressure-diuresis and natriuresis relationships. These effects were abolished by PD. TA decreased urinary cyclic GMP excretion. After pretreatment with PD, this decrease was reversed to an increase which was also observed in animals receiving PD alone. In conclusion, renal AT2 receptors oppose the sodium and water excretion induced by acute increases in blood pressure and this action cannot be directly explained by changes in cyclic GMP.  (+info)

Endothelin mediates renal vascular memory of a transient rise in perfusion pressure due to NOS inhibition. (5/1093)

We investigated the renal responses to NO synthase (NOS) inhibition with N-monomethyl-L-arginine (L-NMA; 30 mg/kg) in anesthetized rats in which renal perfusion pressure (RPP) to the left kidney was mechanically adjusted. Acute L-NMA increased blood pressure (BP, approximately 20%) and renal vascular resistance (RVR) rose ( approximately 50%) in the right kidneys that were always exposed to high RPP. In group 1, the left kidney was exposed to a transient increase (5 min) in RPP which was then normalized, and the rise in RVR was similar to the right kidney. In group 2 the left kidney was never exposed to high RPP, and the rise in RVR was attenuated relative to the right kidney. In group 3, rats were pretreated with the endothelin (ET) receptor antagonist Bosentan, immediately before exposure of the left kidney to a transient increase in RPP, and the rise in RVR was also attenuated relative to the right kidney. NOS inhibition resulted in a natriuresis and diuresis in the right kidneys, and approximately 50% of the natriuresis persisted in the left kidney of group 2, in the absence of any rise in RPP. ET antagonism completely prevented the natriuresis and diuresis in response to acute L-NMA in both left and right kidneys. These data suggest that transient exposure to high RPP by NOS inhibition prevents an appropriate vasodilatory response when RPP is lowered, due to the intrarenal action of ET.  (+info)

Enhanced natriuretic response to neutral endopeptidase inhibition in heart-transplant recipients. (6/1093)

Heart-transplant recipients (Htx) generally present with body fluid and sodium handling abnormalities and hypertension. To investigate whether neutral endopeptidase inhibition (NEP-I) increases endogenous atrial natriuretic peptide (ANP) and enhances natriuresis and diuresis after heart transplantation, ecadotril was given orally to 8 control subjects and 8 matched Htx, and levels of volume-regulating hormones and renal water, electrolyte, and cyclic guanosine monophosphate (cGMP) excretions were monitored for 210 minutes. Baseline plasma ANP, brain natriuretic peptide (BNP), and cGMP were elevated in Htx, but renin and aldosterone, like urinary parameters, did not differ between groups. NEP-I increased plasma ANP (Htx, 20.6+/-2.3 to 33.2+/-5.9 pmol/L, P<0.01; controls, 7.7+/-1. 2 to 10.6+/-2.6 pmol/L) and cGMP, but not BNP. Renin decreased similarly in both groups, whereas aldosterone decreased significantly only in Htx. Enhanced urinary sodium (1650+/-370% versus 450+/-150%, P=0.01), cGMP, and water excretions were observed in Htx and urinary cGMP positively correlated with natriuresis in 6 of the Htx subjects. Consistent with a normal circadian rhythm of blood pressure, without excluding a possible effect of NEP-I, mean systemic blood pressure increased similarly in both groups at the end of the study (6.9+/-2.0% versus 7.4+/-2.8% in controls and Htx). Thus, systemic hypertension, mild renal impairment, and raised plasma ANP levels are possible contributory factors in the enhanced natriuresis and diuresis with NEP-I in Htx. These results support a physiological role for the cardiac hormone after heart transplantation and suggest that long-term studies may be useful to determine the potential of NEP-I in the treatment of sodium retention and water retention after heart transplantation.  (+info)

Impact of the endothelin system on water and sodium excretion in patients with liver cirrhosis. (7/1093)

BACKGROUND: Impaired renal function in patients with liver cirrhosis is a serious complication and is characterized by sodium and water retention in the absence of identifiable specific causes of renal dysfunction. The endothelin system has been shown to be activated in liver cirrhosis and might contribute to impaired renal function. However, the mechanisms leading to an activation of the endothelin system in these patients and the effects of an activated endothelin system on renal function in these patients are as yet unknown. METHODS: To determine the correlation between the activity of the endothelin system and the ability to excrete water and sodium in patients with liver cirrhosis, we measured plasma endothelin-1 concentrations by reversed phase-HPLC followed by an endothelin RIA and performed an oral water load tests in 10 healthy control subjects and 43 patients with liver cirrhosis. In addition, we analysed possible mechanisms/factors like plasma endotoxin that might contribute to the activation of the endothelin system in liver cirrhosis. RESULTS: This study showed that the endothelin system is activated in patients with liver cirrhosis in a disease-stage-dependent manner. Patients with Child C liver cirrhosis have a 5.45-fold increased plasma ET-1 concentration compared to healthy controls, whereas plasma ET-1 is only increased 2.74-fold in Child A patients. An oral water load test revealed a highly significant (P < 0.0001) inverse correlation between the plasma endothelin-1 concentrations and the ability to excrete a given water load. Plasma endotoxin, a well-known stimulus of ET-1, is significantly (P < 0.03) correlated with plasma ET-1 in cirrhotic patients. The ET-1 concentrations in the ascites of patients with liver cirrhosis were lower and not related to plasma ET-1. CONCLUSION: The activity of the endothelin system in patients with liver cirrhosis depends on the severity of liver impairment. Plasma endotoxin might be an important stimulus of the endothelin system in liver cirrhosis. We observed a highly significant inverse correlation between the plasma endothelin-1 concentrations and the ability to excrete a given water and sodium load, suggesting that the endothelin system plays a role in the regulation of water excretion in patients with liver cirrhosis.  (+info)

Altered pressure-natriuresis in obese Zucker rats. (8/1093)

It has not been examined whether the pressure-natriuresis response is altered in the insulin-resistant condition. Furthermore, despite an important role of nitric oxide (NO) in modulating pressure-natriuresis, no investigations have been conducted assessing the renal interstitial NO production in insulin resistance. The present study examined whether pressure-natriuresis was altered in insulin-resistant obese Zucker rats (OZ) and assessed the cortical and medullary nitrate/nitrite (NOx) levels with the use of the renal microdialysis technique. In OZ, serum insulin/glucose ratio (23.0+/-4.0x10(-8), n=9) and blood pressure (119+/-3 mm Hg) were greater than those in lean Zucker rats (LZ; 7.0+/-1.9x10(-8) and 103+/-4 mm Hg, n=9). The pressure-natriuresis curve in OZ was shifted to higher renal perfusion pressure (RPP), and the slope was blunted compared with that in LZ (0.073+/-0.015 vs 0.217+/-0.047 microEq/min kidney weight/mm Hg, P<0.05). The basal renal NOx level was reduced in OZ (cortex, 4.032+/-0.331 micromol/L; medulla, 4. 329+/-0.515 micromol/L) compared with that in LZ (cortex, 7.315+/-1. 102 micromol/L; medulla: 7.698+/-0.964 micromol/L). Furthermore, elevating RPP increased the medullary NOx in LZ, but this pressure-induced response was lost in OZ. Four-week treatment with troglitazone, an insulin-sensitizing agent, improved hyperinsulinemia, systemic hypertension, and basal renal NOx levels (cortex, 5.639+/-0.286 micromol/L; medulla, 5.978+/-0.284 micromol/L), and partially ameliorated the pressure-natriuresis curves; the slope of pressure-natriuresis curves and elevated RPP-induced NOx, however, were not corrected. In conclusion, our study suggests that insulin resistance is closely associated with abnormal pressure-natriuresis and hypertension. These deranged renal responses to insulin resistance are most likely attributed to impaired medullary NO production within the medulla.  (+info)

Abnormal pressure natriuresis. A cause or a consequence of hypertension? | HypertensionAbnormal pressure natriuresis. A cause or a consequence of hypertension? | Hypertension
In all forms of chronic hypertension, the renal-pressure natriuresis mechanism is abnormal because sodium excretion is the same as in normotension despite the increased blood pressure. However, the importance of this resetting of pressure natriuresis as a cause of hypertension is controversial. Theoretically, a resetting of pressure natriuresis could necessitate increased blood pressure to maintain sodium balance or it could occur secondarily to hypertension. Recent studies indicate that, in several models of experimental hypertension (including angiotensin II, aldosterone, adrenocorticotrophic hormone, and norepinephrine hypertension), a primary shift of renal-pressure natriuresis necessitates increased arterial pressure to maintain sodium and water balance. In genetic animal models of hypertension, there also appears to be a resetting of pressure natriuresis before the development of hypertension. Likewise, essential hypertensive patients exhibit abnormal pressure natriuresis, although the ...
Acute growth hormone administration induces antidiuretic and antinatriuretic effects and increases phosphorylation of NKCC2Acute growth hormone administration induces antidiuretic and antinatriuretic effects and increases phosphorylation of NKCC2
Growth hormone (GH) has antidiuretic and antinatriuretic effects in rats and humans, but the molecular mechanisms responsible for these effects are unknown. The aim of this study was to investigate the mechanisms behind the acute renal effects of GH in rats. Female rats received rat (r)GH (2.8 mg/kg sc) or saline and were placed in metabolic cages for 5 h. Urinary excretion of electrolytes and urinary volume were reduced after rGH injection, while urine osmolality was increased. Creatinine and lithium clearance remained unchanged, suggesting that rGH increases reabsorption in segments distal to the proximal tubule. Total plasma insulin-like growth factor I (IGF-I) levels did not change, while cortical IGF-I mRNA abundance was increased. The relative abundance of total and Ser(256)-phosphorylated aquaporin 2 was found to be unchanged by immunoblotting, whereas a significant increase of Thr(96) and Thr(101)-phosphorylated NKCC2 (renal Na(+), K(+), 2Cl(-) cotransporter) was found in the inner ...
Renal adrenoceptor mediation of antinatriuretic and renin secretion responses to low frequency renal nerve stimulation in the...Renal adrenoceptor mediation of antinatriuretic and renin secretion responses to low frequency renal nerve stimulation in the...
We evaluated renal adrenoceptor mediation of the renin secretion and antinatriuretic responses to low frequency (1.0 Hz) electrical stimulation of the renal nerves in the dog using renal a-adrenoceptor blockade with phentolamine {a-i/a-i), prazosin (a,), yohimbine (a2), and rauwolscine (a2), and /3-adrenoceptor blockade with d,/-propranolol OS1//S2) and atenolol (/?,). In all animals studied, renal blood flow and glomerular filtration rate remained constant throughout the experiment. In 11 dogs, low frequency renal nerve stimulation decreased urinary sodium excretion (119 ± 13 to 86 ± 18 jiEq/min) and increased renin secretion (79 ± 22 to 348 ± 73 ng/ min). Renal arterial infusion of phentolamine (2-10 Mg/kg per min) prevented the antinatriuresis but did not change the response of renin secretion (96 ± 46 to 412 ± 93 ng/min). In six dogs, renal arterial infusion of prazosin (0.7 ^g/kg per min) similarly blocked the antinatriuretic but not the renin secretion responses to low frequency renal nerve
Hypertension Induced by Chronic Renal Adrenergic Stimulation Is Angiotensin Dependent | HypertensionHypertension Induced by Chronic Renal Adrenergic Stimulation Is Angiotensin Dependent | Hypertension
It is well established that acute renal adrenergic stimulation decreases urinary sodium excretion. The antinatriuretic effects of renal adrenergic stimulation are mediated directly by (1) an influence on renal tubular cells to promote sodium reabsorption and (2) vasoconstriction, which decreases GFR and renal blood flow. Additionally, activation of the renal nerves increases renin release at a level of stimulation below that required to increase sodium reabsorption and cause vasoconstriction. Therefore, since Ang II has potent vasoconstrictor and antinatriuretic effects, it would be expected that some of the renal actions associated with renal adrenergic stimulation are mediated indirectly via Ang II generation. Unfortunately, the design of many experimental studies does not allow a quantitative assessment of the multiple pathways by which adrenergic stimulation alters sodium excretion and renal hemodynamics, especially under chronic conditions. In the present study, the renal actions of acute ...
JCI - Distinct roles for the kidney and systemic tissues in blood pressure regulation by the renin-angiotensin systemJCI - Distinct roles for the kidney and systemic tissues in blood pressure regulation by the renin-angiotensin system
The important role of the kidney in regulation of blood pressure has been long recognized (29), and the relationship between alterations in systemic blood pressure and changes in renal sodium excretion is well documented (30). For example, an elevation in perfusion pressure in the renal artery results in a rapid increase in sodium and water excretion by the kidney, so-called pressure natriuresis (30). Based on such observations, Guyton and coworkers suggested that whenever arterial pressure is elevated, activation of this pressure-natriuresis mechanism will cause sufficient excretion of sodium and water to return systemic pressures to normal (31). Because of its potent actions to modulate renal sodium excretion, angiotensin II has been implicated as a major determinant of these pressure-natriuresis relationships (19, 32). These actions may be mediated by direct effects of AT1 receptors on renal resistance vessels and epithelial cells or indirectly through stimulation of aldosterone production ...
Vessel Dilator Enhances Sodium and Water Excretion and Has Beneficial Hemodynamic Effects in Persons With Congestive Heart...Vessel Dilator Enhances Sodium and Water Excretion and Has Beneficial Hemodynamic Effects in Persons With Congestive Heart...
Vessel dilator caused a significant diuresis in persons with CHF. The 2- to 13-fold increase in urine volume in the CHF subjects is nearly identical to the amount of diuresis (4- to 12-fold) found in healthy humans given vessel dilator,1 suggesting that the effects of vessel dilator are not blunted in humans with CHF. Vessel dilator also stimulated a natriuresis (3- to 4-fold) in the human subjects with CHF that was similar to the amount of natriuresis previously observed in healthy human subjects secondary to vessel dilator.1 The ability of vessel dilator to increase the excretion of sodium and the filtration fraction of sodium (FENa+) without enhancing creatinine clearance or glomerular filtration rate suggests that it is inhibiting the reabsorption of sodium in the renal tubules of persons with CHF. Vessel dilator is known to inhibit sodium reabsorption in the inner medullary collecting duct and renal tubules by inhibiting their Na+-K+-ATPases secondary to its ability to enhance the synthesis ...
Salt, Hypertension and Cardiovascular Disease: the Connection | Indonesian Journal of CardiologySalt, Hypertension and Cardiovascular Disease: the Connection | Indonesian Journal of Cardiology
There is a relationship between Blood Pressure (BP) and natriuresis which maintains sodium bal-ance and extra cellular fluid volume. An impaired ability of the kidney to excrete sodium, requires an increase in BP to increase natriuresis and correct sodium balance resulting in HT. Much evidence suggests, that in those who develops high BP, there is an underlying defect in the ability of the kidney to excrete salt and that the greater compensatory response required to restore sodium balance is the cause for the increase in BP ...
Definition: Long-Term Control MedicineDefinition: Long-Term Control Medicine
Medicamentos de control). Theres a reason for this medicines name: If your doctor prescribed it for your asthma, you need to take it every day, over a long period of time, to control the condition. Long-term control medicines are sometimes also called controller or maintenance medicines.. Long-term control medicine works slowly over time to keep the airways in the lungs open and clear. It may take days or weeks for long-term control medicine to start working and keep the airways from becoming swollen and narrow. Thats why people need to take it each day, even when they feel OK.. ...
Role of Kinins in the Control of Renal Papillary Blood Flow, Pressure Natriuresis, and Arterial Pressure | Circulation ResearchRole of Kinins in the Control of Renal Papillary Blood Flow, Pressure Natriuresis, and Arterial Pressure | Circulation Research
In the present study, Hoe140 reduced renal PBF at high RPP and improved PBF autoregulation, without any effects on the renal cortical circulation. This is consistent with previous reports showing that other B2 antagonists lowered PBF.7 The source of renal medullary kinins is unknown, because most of the renal kallikrein is produced in the connecting tubule, within the renal cortex.1 The effects of Hoe140 on PBF are compatible with a vascular source from which kinins can reach the renal interstitial fluid, where bradykinin is present.17 18 Interestingly, kinins can be synthesized and released by endothelial cells and mediate part of the endothelial shear stress-induced changes in blood flow.11 12 It has been previously reported that NO synthesis blockade abolishes the pressure-induced increases in medullary blood flow, and it has been hypothesized that as arterial pressure rises, endothelial shear stress increases in the preglomerular vasculature, releasing NO and originating the intrarenal ...
Comparison of the natriuretic response to atriopeptin III and loop diuretic in the isolated perfused rat kidney | Clinical...Comparison of the natriuretic response to atriopeptin III and loop diuretic in the isolated perfused rat kidney | Clinical...
1. Isolated rat kidneys were perfused at a constant perfusion pressure of 90 mmHg to study the natriuretic effects of atriopeptin III (AP-III) and to compare these effects with those of frusemide. AP-III (1 μg) or frusemide (1 mg) were added to the perfusate (100 ml) after two 15 min control collection periods.. 2. Compared with the control group, AP-III and frusemide increased urinary sodium excretion (UNaV, 5.6 ± 1.1 and 4.6 ± 0.6 vs control 1.8 ± 0.3 μmol min−1 g−1, mean ± sem, P , 0.01 and P , 0.05, respectively), fractional sodium excretion (FENa, 4.8 ± 1.1 and 6.7 ± 0.8 vs control 2.0 ± 0.2%, P , 0.05 and P , 0.001, respectively) and potassium excretion (UKV, 3.2 ± 0.3 and 3.0 ± 0.3 vs control 1.5 ± 0.3 μmol min−1 g−1, both P , 0.01). However, AP-III, but not frusemide, increased glomerular filtration rate (820 ± 55 vs 590 ± 24 μl min−1 g−1, P , 0.01) and urine flow rate (V 97.5 ± 8.0 vs 44.1 ± 5.2 μl min−1 g−1, P , 0.001). Calculated distal delivery of ...
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Mapping studies have identified many QTLs affecting BP in genetically hypertensive rats, and their isolation in congenic strains has been the main approach used for their further characterization (20). Apart from genetic analysis, congenic strains provide a powerful tool for identifying relevant intermediary phenotypes, since they only differ from control (parental) strains for a small fraction of the genome. Thus any differences seen are more likely to be involved in the physiological pathway(s) that regulates the trait of interest. In this study, we demonstrate for the first time that the rat chromosome 1 BP QTL region also influences pressure-natriuresis relationship, salt sensitivity, and most probably sympathetic activation following salt loading. These findings may be related and pertinent to the effect on BP.. Pressure-natriuresis was studied using the classic method designed by Roman and Cowley (23), which one allows to maintain, at a fixed level, most of the extrarenal factors that ...
Rapid Atrial Pacing in Cardiac Denervated Dogs Causes Sodium Retention and Not Natriuresis | Clinical Science | Portland PressRapid Atrial Pacing in Cardiac Denervated Dogs Causes Sodium Retention and Not Natriuresis | Clinical Science | Portland Press
T D M Williams, K P Walsh, M I M Noble, A J Drake-Holland, E Pitts, S L Lightman, R Sutton; Rapid Atrial Pacing in Cardiac Denervated Dogs Causes Sodium Retention and Not Natriuresis. Clin Sci (Lond) 1 January 1988; 75 (s19): 31P. doi: https://doi.org/10.1042/cs075031P. Download citation file:. ...
Multiple Sclerosis Clinical Trial 2016-064 - Lahey Hospital & Medical Center, Burlington & PeabodyMultiple Sclerosis Clinical Trial 2016-064 - Lahey Hospital & Medical Center, Burlington & Peabody
This study is for patients with Relapsing Remitting Multiple Sclerosis who are on a first-line treatment. Patients who are randomized into the experiment group will have to follow a 2,000 daily intake of sodium diet. During the duration of the study there will be four 24 hour urine sodium excretion, dietary questionnaire, and dietitian-led sessions.
Fractional Excretion of Sodium - Trip DatabaseFractional Excretion of Sodium - Trip Database
Find all the evidence you need on Fractional Excretion of Sodium via the Trip Database. Helping you find trustworthy answers on Fractional Excretion of Sodium | Latest evidence made easy
What is Diuresis? (with pictures)What is Diuresis? (with pictures)
Diuresis is an increase in the production of urine by the kidneys. Usually connected with an increase in urine, diuresis can cause...
Response of superficial proximal convoluted tubule to decreased and increased renal perfusion pressure. In vivo microperfusion...Response of superficial proximal convoluted tubule to decreased and increased renal perfusion pressure. In vivo microperfusion...
Although urinary sodium excretion is positively influenced by acute changes in renal perfusion pressure, micropuncture studies show highly conflicting results concerning the response of superficial proximal tubule sodium reabsorption to changes in renal perfusion pressure. In the present study, the changes of superficial proximal reabsorption to decreased and increased renal perfusion pressure were determined in rats by an in vivo microperfusion method. In vivo microperfusion was selected as the method to determine the proximal sodium reabsorption because this method made it possible to deliver a constant fluid and electrolyte load to the proximal tubule without the influence of possible changes of glomerular filtration rate. Renal perfusion pressure was decreased from normal pressure by inflating a suprarenal aortic cuff and was increased from the normal level by the occlusion of celiac and mesenteric arteries and the infrarenal aorta. Although fractional excretion of sodium (FENa) in the urine ...
ASSA14-03-08 Gastrin and D1 Dopamine Receptor Interact to Induce Natriuresis and Diuresis | HeartASSA14-03-08 Gastrin and D1 Dopamine Receptor Interact to Induce Natriuresis and Diuresis | Heart
Result Gastrin infusing WKY rats via renal artery induced natriuresis and diuresis, which was blocked in the presence of CI988, a gastrin receptor blocker. Similarly, effect hereinbefore of fenoldopam, a D1-like receptor agonist, was blocked by D1-like receptor antagonist, SCH23390, indicating gastrin and fenoldopam play natriuretic and diuretic effect through individual receptors. Lower dosages of gastrin or fenoldopam failed to induce natriuresis and diuresis alone, while putting together induced the effects. The above-mentioned effects were lost in SHRs. Natriuresis and diuresis was partially blocked by SCH23390 or CI988, indicating the interaction between gastrin and D1-like receptor. Stimulation of either receptor increased the expression of the other and inhibited Na+-K+-ATPase activity, while the inhibitory effect of Na+-K+-ATPase activity was partially blocked through its corresponding receptors due to respective existence of SCH23390 and CI988.. ...
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Nonsteroidal anti-inflammatory drugs have been shown to decrease the natriuretic response to loop diuretics in many but not all studies. Recently, indomethacin was shown not to affect the natriuretic response to the new loop diuretic torasemide in healthy volunteers. Inasmuch as sodium balance has been reported to modify the effect of indomethacin on furosemide-induced natriuresis in dogs, we investigated the effect of indomethacin, under two sodium balances (50 and 150 mEq/day), on the natriuretic response to two doses of torasemide in six healthy volunteers. Under the low sodium diet, indomethacin reduced the natriuretic response to torasemide like that to furosemide. In contrast, on the normal sodium diet, indomethacin failed to affect the natriuretic response to torasemide. Indomethacin reduced base-line and diuretic-induced increase in plasma renin activity, plasma angiotensin II levels and urinary excretion of prostaglandin 6-keto F1 alpha to a similar extent under the two sodium diets. ...
Neuropeptide Y: a novel renal peptide with vasoconstrictor and natriuretic activity | Clinical ScienceNeuropeptide Y: a novel renal peptide with vasoconstrictor and natriuretic activity | Clinical Science
1. A novel vasoconstrictor peptide, neuropeptide Y (NPY), has been identified in considerable quantities in the renal artery and kidney. Within the kidney, NPY was confined to the cortex and corticomedullary interface, the regions where the juxtaglomerular apparatus is most numerous.. 2. In the isolated perfused rat kidney, NPY caused a prompt dose-dependent increase in perfusion pressure and reduction in flow, with only a small fall in glomerular filtration rate (GFR). In spite of the reduced renal perfusion, a dose-dependent natriuresis was observed. This response contrasts to the response of this preparation to noradrenaline, which causes sodium reabsorption.. 3. The presence of a potent vasoconstrictor and natriuretic peptide within the rat renovascular system suggests that it may play a significant role in the control of renal function.. ...
Urine Chloride/Creatinine Ratio for Estimation of Urine Sodium - Full Text View - ClinicalTrials.govUrine Chloride/Creatinine Ratio for Estimation of Urine Sodium - Full Text View - ClinicalTrials.gov
Level of salt intake has an important impact in patients with high blood pressure or congestive heart failure. Despite this there is no convenient way for doctors or patients to assess their salt intake other than diet recall, which is unreliable, or measurement of sodium excretion in a 24 hour collection of urine, which is very inconvenient. As a result, salt intake is not monitored in most patients.. 2 innovations might enable a more convenient assessment of salt intake. A titrator stick that measures chloride ion concentration (chloride and sodium concentrations correlate strongly with each other), and a titrator stick that measures urine creatinine. The latter enables estimation of 24 hour excretion from a single sample of urine. In assessing sodium intake, a measurement that provides an approximation of urine sodium intake would be of considerable clinical value. In this study, we shall compare the estimation of urine sodium excretion measured by a laboratory with estimation of sodium ...
Metabolic Cages for Rodent | Sabale SystemMetabolic Cages for Rodent | Sabale System
NuAire Metabolic cages Rodent, Innovive Rodent metabolic cages, Metabolic Cages Rodent harvardapparatus, Metabolic Cage Rodent VWR, Allentown Rodent Metabolic Cage, Labconco Rodent metabolic cages Thermofisher
LongevityMap variantLongevityMap variant
This gene encodes a serine/threonine protein kinase that plays an important role in cellular stress response. This kinase activates certain potassium, sodium, and chloride channels, suggesting an involvement in the regulation of processes such as cell survival, neuronal excitability, and renal sodium excretion. High levels of expression of this gene may contribute to conditions such as hypertension and diabetic nephropathy. Several alternatively spliced transcript variants encoding different isoforms have been noted for this gene. [provided by RefSeq, Jan 2009 ...
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Armentrout, P.B.; Rodgers, M.T., An Absolute Sodium Cation Affinity Scale: Threshold Collision-Induced Dissociation Experiments and ab Initio Theory, J. Phys. Chem A, 2000, 104, 11, 2238, https://doi.org/10.1021/jp991716n . 16 matching species were found. For each matching species the following will be displayed: ...
Managing COPD: Medicines for Long-Term ControlManaging COPD: Medicines for Long-Term Control
You may need several types of medicine to control your COPD symptoms. You may take some of these medicines using an inhaler. Others you may take by mouth.
Managing COPD: Medicines for Long-Term ControlManaging COPD: Medicines for Long-Term Control
You may need several types of medicine to control your COPD symptoms. You may take some of these medicines using an inhaler. Others you may take by mouth.
Pretraga | FENAPretraga | FENA
Federalna novinska agencija je punopravni član: Evropske alijanse novinskih agencija (EANA), Asocijacije balkanskih novinskih agencija (ABNA) i Vijeća za štampu u BiH ...
Cardio-renal-endocrine dynamics during stepwise infusion of physiologic and pharmacologic concentrations of atrial natriuretic...Cardio-renal-endocrine dynamics during stepwise infusion of physiologic and pharmacologic concentrations of atrial natriuretic...
TY - JOUR. T1 - Cardio-renal-endocrine dynamics during stepwise infusion of physiologic and pharmacologic concentrations of atrial natriuretic factor in the dog. AU - Zimmerman, R. S.. AU - Schirger, J. A.. AU - Edwards, B. S.. AU - Schwab, T. R.. AU - Heublein, D. M.. AU - Burnett, J. C.. PY - 1987/1/1. Y1 - 1987/1/1. N2 - Infusion of α-human-atrial natriuretic factor (α-h-ANF) into pentobarbitol anesthesized dogs (n = 10) at 0.0025, 0.005, 0.01, and 0.3 μg/kg/min was performed to differentiate the physiologic actions of atrial natriuretic factor from its pharmacologic actions. The lowest doses of atrial natriuretic factor infusion resulted in circulating levels that were previously produced by 0-10% saline volume expansion. At the lowest infusion rate, circulating ANF increased 31 ± 3 pg/ml, resulting in a significant increase in absolute sodium excretion, fractional excretion of sodium, and fractional excretion of lithium, and a significant decrease in urine osmolality. A greater change ...
Mechanisms Controlling Release of Atrial Natriuretic Peptide | SpringerLinkMechanisms Controlling Release of Atrial Natriuretic Peptide | SpringerLink
the myoendocrine cellsin the atria of the mammalian heart synthesize and secrete a hormone called atrial natriuretic peptide (ANP), which causes natriuresis and diuresis. Pharmacological studies in...
Plus itPlus it
Effects of a K+ channel blocker on glomerular filtration rate and electrolyte excretion in conscious rats were observed. Effects of K+ channel modulation on glomerular filtration rate and electrolyte excretion were studied using the adenosine-triphosphate- (ATP)-sensitive K+ channel blocker 4-morpholinecarboximidine-N-1-adamantyl-N-cyclohexylhydr ochloride (U-37883A) in conscious rats previously equipped with catheters for clearance studies. In saline-loaded rats, i.v. doses of U-37883A of 1.7, 5.0 and 15 mg/kg increased absolute and fractional Na+ excretion dose-dependently without changing K+ excretion. The glomerular filtration rate remained constant during diuresis. In water-loaded (hypotonic dextrose) rats, free-water clearance studies revealed that the ATP-sensitive K+ channel blocker significantly decreased an index of solute reabsorption (free-water clearance adjusted for chloride clearance) in the diluting segment during peak natriuretic activity. In addition, U-37883A significantly ...
Loss of Collectrin, an Angiotensin-Converting Enzyme 2 Homolog, Uncouples Endothelial Nitric Oxide Synthase and Causes...Loss of Collectrin, an Angiotensin-Converting Enzyme 2 Homolog, Uncouples Endothelial Nitric Oxide Synthase and Causes...
Collectrin is an "orphan" member of the renin-angiotensin system with a previously unrecognized role in cardiovascular and renal physiology. We demonstrate that loss of collectrin results in hypertension, altered pressure natriuresis, and superoxide-dependent augmented salt sensitivity. We further demonstrate that deletion of collectrin results in endothelial dysfunction, which is associated with eNOS uncoupling, increased O2· − production, and decreased NO availability, likely as a result of impaired cellular uptake of l-arginine substrate. Our data suggest that collectrin plays a protective role against conditions that predispose to the hypertensive state by maintaining a balance of NO and O2· − through its role in facilitating the cellular uptake of l-arginine. It is worth noting that we previously reported that collectrin KO mice have normal development, are able to compensate for renal wasting of amino acids by increased liver synthesis of nonessential amino acids, and are able to ...
A Randomized, Double-blind, Controlled, Crossover Study to Evaluate the Sodium Excretion of LCZ696 in Patients With Stable...A Randomized, Double-blind, Controlled, Crossover Study to Evaluate the Sodium Excretion of LCZ696 in Patients With Stable...
This trial investigated the sodium excretion of LCZ696 in patients with stable heart failure, in patients with hypertension, and in healthy volunteers.
SGK1 serum/glucocorticoid regulated kinase 1 [Homo sapiens (human)] - Gene - NCBISGK1 serum/glucocorticoid regulated kinase 1 [Homo sapiens (human)] - Gene - NCBI
This gene encodes a serine/threonine protein kinase that plays an important role in cellular stress response. This kinase activates certain potassium, sodium, and chloride channels, suggesting an involvement in the regulation of processes such as cell survival, neuronal excitability, and renal sodium excretion. High levels of expression of this gene may contribute to conditions such as hypertension and diabetic nephropathy. Several alternatively spliced transcript variants encoding different isoforms have been noted for this gene. [provided by RefSeq, Jan 2009 ...
Can the generic form of Prilosec affect the prostate? Reduce urine flow?Can the generic form of Prilosec affect the prostate? Reduce urine flow?
1 Answer (question resolved) - Posted in: prilosec, generic, prostate, urine - Answer: From my review of Prilosec decreased urine flow is not listed ...
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The effects of a stressful environmental stimulus (air stress) on mean arterial pressure, heart rate, renal sympathetic nerve activity, and renal function were studied in conscious deoxycorticosterone acetate-sodium chloride (DOCA-NaCl) hypertensive rats, sham DOCA-NaCl normotensive rats, and DOCA-NaCl rats with renal denervation. In conscious DOCA-NaCl hypertensive rats, air stress decreased urine flow rate [36% from 17.9 +/- 3.0 microliter X min-1 X 100 g body wt-1 (BW)], urinary sodium excretion (39% from 3.1 +/- 0.5 microeq X min-1 X 100 g BW-1), fractional water excretion (24% from 4.72 +/- 1.00%), and fractional sodium excretion (28% from 5.72 +/- 1.08%) and increased renal sympathetic nerve activity (94% from 8.3 +/- 0.6 integrator resets/min), but no changes occurred in glomerular filtration rate (-15% from 0.40 +/- 0.06 ml X min-1 X 100 g BW-1) or effective renal plasma flow (-7% from 2.50 +/- 0.53 ml X min-1 X 100 g BW-1). Air stress had no effect on these measures in conscious sham ...
Atrial natriuretic factor financial definition of atrial natriuretic factorAtrial natriuretic factor financial definition of atrial natriuretic factor
Definition of atrial natriuretic factor in the Financial Dictionary - by Free online English dictionary and encyclopedia. What is atrial natriuretic factor? Meaning of atrial natriuretic factor as a finance term. What does atrial natriuretic factor mean in finance?
Haemodynamic, renal sodium handling, and neurohormonal effects of acute administration of low dose losartan, an angiotensin II...Haemodynamic, renal sodium handling, and neurohormonal effects of acute administration of low dose losartan, an angiotensin II...
The results of this preliminary study confirm previous findings that preascitic cirrhotic patients have subtle sodium retention when placed on a 200 mmol sodium as opposed to a 100 mmol sodium per day intake,1 2 23 manifested as a reduced urinary sodium excretion, associated with suppression of systemic RAAS in the supine posture. The acute use of a low dose angiotensin II receptor antagonist resulted in normalisation of this subtle sodium handling abnormality in preascitic cirrhotic patients, despite unchanged renal and systemic haemodynamics.. A 200 mmol sodium per day diet was chosen for this study for several reasons. Preascitic cirrhotic patients have previously been shown to come into a steady state of subtle sodium retention after four days of this sodium intake,2 and therefore the study would not require a long run in period. Secondly, this level of sodium intake, although higher than that contained in the usual "no added salt diet of 100-130 mmol sodium per day" that the patients were ...
Most recent papers with the keyword Hypertension angiotensin renin sodium retention salt | Read by QxMDMost recent papers with the keyword Hypertension angiotensin renin sodium retention salt | Read by QxMD
AIMS/HYPOTHESIS: Glitazones are powerful insulin sensitisers prescribed for the treatment of type 2 diabetes. Their use is, however, associated with fluid retention and an increased risk of congestive heart failure. We previously demonstrated that pioglitazone increases proximal sodium reabsorption in healthy volunteers. This study examines the effects of pioglitazone on renal sodium handling in individuals prone to insulin resistance, i.e. those with diabetes and/or hypertension. METHODS: In this double-blind randomised placebo-controlled four-way crossover study, we examined the effects of pioglitazone (45 mg daily during 6 weeks) or placebo on renal, systemic and hormonal responses to changes in sodium intake in 16 individuals, eight with type 2 diabetes and eight with hypertension ...
Reduced Renal Papillary Plasma Flow in Non-Ascitic Cirrhotic Rats | Clinical Science | Portland PressReduced Renal Papillary Plasma Flow in Non-Ascitic Cirrhotic Rats | Clinical Science | Portland Press
1. The purpose of the present investigation was to determine whether an abnormality of the renal papillary circulation is present in a well-established model of cirrhosis without ascites (carbon tetrachloride/phenobarbital).. 2. Compared with the control animals, cirrhotic rats showed a reduced diuretic (61.0 ±5.1 versus 18.0 ±2.5%) and natriuretic (67.8 ±8.3 versus 29.6 ±3.6%) response to a volume expansion (3% body weight infusion of 0.9% NaCl). The volume expansion-induced increase in renal interstitial hydrostatic pressure was also blunted in the cirrhotic rats (control 9.3 ±0.9 versus cirrhotic 6.1±1.0 mmHg) and there were no differences in mean arterial blood pressure, renal blood flow or glomerular filtration rate between control and cirrhotic animals.. 3. Papillary plasma flow was determined by the 125I-albumin accumulation technique and expressed as mlmin−1100 g−1. In the basal state, papillary plasma flow was significantly lower in cirrhotic rats (59.1 ±4.4, n = 9) than in ...
NephMadness: Collecting Tubule Region - Principal Cell Group - AJKD BlogNephMadness: Collecting Tubule Region - Principal Cell Group - AJKD Blog
One of the most common causes of a falsely elevated fractional excretion of sodium is diuretics. Diuretics directly increase sodium excretion, increasing the FENa without regard to natural renal sodium handling. The fractional excretion of urea circumvents this by measuring renal handling of urea, a molecule not affected by diuretics. With decreasing renal blood flow the kidney autoregulates to maintain a stable GFR. One of the results for this autoregulation is an increase in the fraction of renal plasma flow that is filtered through the glomerulus, the filtration fraction. The increased filtration fraction means that the serum albumin, which is not filtered, is dissolved in less plasma so is found at a greater concentration and thus exerts increased osmotic pressure drawing water, sodium and urea from the proximal tubule back to the blood. This lowers the excretion of urea. This decreased clearance of urea with decreased effective circulating volume decreases the fractional excretion of urea ...
Atrial natriuretic factor: implications in congestive heart failure and hypertension.Atrial natriuretic factor: implications in congestive heart failure and hypertension.
The physiological actions of the atrial peptide system are discussed in relation to its potential role in the aetiology and treatment of hypertension and congestive heart failure (CHF). Atrial natriuretic factor (ANF) exerts marked natriuretic, diure
Haemodynamic, renal sodium handling, and neurohormonal effects of acute administration of low dose losartan, an angiotensin II...Haemodynamic, renal sodium handling, and neurohormonal effects of acute administration of low dose losartan, an angiotensin II...
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Centers RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.. ...
Effects of Inhibition of NO-Synthesis on Renal Hemodynamics and Sodium Excretion in Patients With Essential Hypertension and...Effects of Inhibition of NO-Synthesis on Renal Hemodynamics and Sodium Excretion in Patients With Essential Hypertension and...
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies. ...
Asthma MedicinesAsthma Medicines
Asthma medicine comes in two main types: quick-relief and long-term control medicines. Even if a child takes a long-term control medicine regularly, quick-relief medicine is still needed to handle flare-ups.
Will Your Eyes Change From Black to Blue..."Will Your Eyes Change From Black to Blue...
Will Your Eyes Change from Black to Blue? by C.C.S.V.I. Ontario on Wednesday, August 31, 2011 at 10:19am Will your Eyes Change from Black to Blue? I am one of the lucky ones. I had the money, and the strength ...
Hypoxanthine plus xanthine oxidase causes profound natriuresis without affecting renal blood flow autoregulationHypoxanthine plus xanthine oxidase causes profound natriuresis without affecting renal blood flow autoregulation
Hypoxanthine plus xanthine oxidase causes profound natriuresis without affecting renal blood flow autoregulation. Background Enhanced superoxide production by xanthine oxidase in ischemia/reperfusion has been implicated in structural damage. The reperfusion phase is accompanied by decreased tubular sodium reabsorption, which has been partly attributed to enhanced action of . In the present study we assessed whether intrarenal increases of accomplished by concomitant intrarenal hypoxanthine and intravenous xanthine oxidase (HX/XO) infusion would decrease or increase sodium excretion, and whether HX/XO infusion could be responsible for the diminished efficacy of renal blood flow (RBF) autoregulation in ischemia/reperfusion. Methods In the first group of Sprague-Dawley rats, renal sodium handling was measured before and during infusion. In the second group, renal hemodynamics and RBF autoregulation were assessed. Results Intrarenal infusion dramatically increased urine flow from 14.5 2.0 L/min to ...
Changes in atrial natriuretic peptide concentrations during intravenous saline infusion in hypoxic cor pulmonaleChanges in atrial natriuretic peptide concentrations during intravenous saline infusion in hypoxic cor pulmonale
Plasma atrial natriuretic peptide in essential hypertension: effects of changes in dietary sodium. Sagnella, Giuseppe A.; Markandu, Nirmala D.; Buckley, Martin G.; Singer, Donald R.J.; Sugden, A. Louise; Shore, Angela C.; MacGregor, Graham A. // British Medical Journal (Clinical Research Edition);8/15/1987, Vol. 295 Issue 6595, p417 Examines the plasma atrial natriuretic peptide in essential hypertension. Effects of changes in dietary intake on plasma atrial peptides; Occurrence of change in plasma concentration of atrial peptide values during the transfer from normal to high sodium diet; Correlation between the fall in... ...
Atrial natriuretic peptide - WikipediaAtrial natriuretic peptide - Wikipedia
Atrial natriuretic peptide (ANP) is a peptide hormone which reduces an expanded extracellular fluid (ECF) volume by increasing renal sodium excretion. ANP is synthesized, and secreted by cardiac muscle cells in the walls of the atria in the heart. These cells contain volume receptors which respond to increased stretching of the atrial wall due to increased atrial blood volume. ANP is one of a family of nine natriuretic peptides: seven are atrial in origin. ANP acts on the kidney to increase sodium and water excretion (natriuresis) in the following ways: 1) it dilates the glomerular afferent and constrict efferent arterioles, and relaxes the mesangial cells. This increases pressure in the glomerular capillaries, increasing the glomerular filtration rate (GFR), resulting in an increased amount of sodium and water being filtered and excreted. 2) It increases blood flow through the vasa recta, which washes the solutes sodium chloride (NaCl) and urea out of the medullary interstitium - the lower ...
இதயியச் சோடியச்சிறுநீர்மைப் புரதக்கூறு - தமிழ் விக்கிப்பீடியாஇதயியச் சோடியச்சிறுநீர்மைப் புரதக்கூறு - தமிழ் விக்கிப்பீடியா
திறன்மிகு நாள விரிப்பியான (Vasodilator) இதயியச் சோடியச்சிறுநீர்மைப் புரதக்கூறு [Atrial natriuretic peptide; (ANP), atrial natriuretic factor; (ANF), atrial natriuretic hormone; (ANH), Cardionatrine, Cardiodilatine; (CDD), atriopeptin], இதயத்தசைச் செல்களால் சுரக்கப்படும் புரதக்கூற்று இயக்குநீராகும்[2][3][4]. இப்புரதக்கூறானது உடலின் நீர், சோடியம், பொட்டாசியம், கொழுப்புத் திசுக்களில் உள்ள கொழுப்பு ஆகியவற்றின் சமநிலையைக் கட்டுபடுத்துவதில் ஈடுபட்டுள்ளது; இரத்தத்தின் கன அளவு ...
Effect of estrogen receptor modulator tamoxifen on blood pressure, plasma renin activity, and renal sodium excretion. - PubMed...Effect of estrogen receptor modulator tamoxifen on blood pressure, plasma renin activity, and renal sodium excretion. - PubMed...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
DISEASES - NPPADISEASES - NPPA
NPPA [ENSP00000365663]. Cardiodilatin-related peptide; Hormone playing a key role in cardiovascular homeostasis through regulation of natriuresis, diuresis, and vasodilation. Also plays a role in female pregnancy by promoting trophoblast invasion and spiral artery remodeling in uterus. Specifically binds and stimulates the cGMP production of the NPR1 receptor. Binds the clearance receptor NPR3; Belongs to the natriuretic peptide family.. Synonyms: NPPA, B0ZBE8, P01160, ANP, B0ZBE8p .... Linkouts: STRING Pharos UniProt OMIM ...
antiarrhythmic peptide - AAP Summary Report | CureHunterantiarrhythmic peptide - AAP Summary Report | CureHunter
antiarrhythmic peptide: atrial peptide from bovine atria; hexapeptide composed of hydroxyproline(1), proline(1), glycine(3) & alanine(1); both N-terminal & carboxy-terminal residues are glycine
RightAnswer Knowledge SolutionsRightAnswer Knowledge Solutions
TOXICOLOGY: GI: Indomethacin is a direct GI irritant, and the inhibition of prostaglandin synthesis interferes with the maintenance of the GI barrier. Inhibition of thromboxane A2 in platelets prolongs bleeding time and predisposes to GI bleeding. RENAL: Decreases in prostaglandins I2 and E2, which have vasodilatory and natriuretic effects in the kidney that can lead to salt and water retention, and renal failure ...
Asthma Medicines (for Parents) - Cook ChildrensAsthma Medicines (for Parents) - Cook Children's
Asthma medicine comes in two main types: quick-relief and long-term control medicines. Even if a child takes a long-term control medicine regularly, quick-relief medicine is still needed to handle flare-ups.
Nephron Power: TOPIC DISCUSSION: FENA less than one causes!Nephron Power: TOPIC DISCUSSION: FENA less than one causes!
Although the test was designed originally in Oliguric patients. So how much use we have of it. Who knows! but above list is usually where we see FeNa,1 ...
Fena Wijaya | Access ConsciousnessFena Wijaya | Access Consciousness
I am Fena Wijaya, an Indonesian Energy Healer, and a Joyfull Life Coach. Working many years in these sectors provides me with versatile capabilities in coaching people to create their goal in their life and living. And one day, I meet someone, she introducing Access Counsiousness to me, and she said to me this Access is different modality from others. I am so interesting to find out, I took the bars dan foundation class.... OMG, Im in love with the tools... With energy we can change the world and we Empowering people to know that they know.. And I start having my classes and commited to it. Play with all people in this world.. Creating together.. For me, I really enjoy to share happines and counsciousness.. I am Bars & Facelift Facilitator, Stepping intro being you facilitator.. ...
Fena Wijaya | Access ConsciousnessFena Wijaya | Access Consciousness
I am Fena Wijaya, an Indonesian Energy Healer, and a Joyfull Life Coach. Working many years in these sectors provides me with versatile capabilities in coaching people to create their goal in their life and living. And one day, I meet someone, she introducing Access Counsiousness to me, and she said to me this Access is different modality from others. I am so interesting to find out, I took the bars dan foundation class.... OMG, Im in love with the tools... With energy we can change the world and we Empowering people to know that they know.. And I start having my classes and commited to it. Play with all people in this world.. Creating together.. For me, I really enjoy to share happines and counsciousness.. I am Bars & Facelift Facilitator, Stepping intro being you facilitator.. ...
Total Viral Load Strategy | U.S. WuXi AppTecTotal Viral Load Strategy | U.S. WuXi AppTec
Learn the advantages of utilizing a total viral load strategy to optimize viral clearance studies. This approach is used to identify the right spike levels.
Clinical Research | Columbia University Department of SurgeryClinical Research | Columbia University Department of Surgery
Columbia University Department of Surgery is conducting hundreds of clinical trials to improve care for many types of conditions.. Use the tool below to find our clinical trials that are currently enrolling new patients. Each listing explains the purpose of the trial, links to the investigators biography, the trials eligibility criteria, and how to get more information.. ...
Dopamine receptorDopamine receptor
Management of heart failureManagement of heart failure
BradykininBradykinin
ACE inhibitorACE inhibitor
Sodium-hydrogen antiporter 3Sodium-hydrogen antiporter 3
UrodilatinUrodilatin
AscitesAscites
Epithelial sodium channelEpithelial sodium channel
NocturiaNocturia
NPR1NPR1
Natriuretic peptideNatriuretic peptide
HydrochlorothiazideHydrochlorothiazide
Progesterone (medication)Progesterone (medication)
CaffeineCaffeine
OmapatrilatOmapatrilat
Osmotic diureticOsmotic diuretic
DeoxyepinephrineDeoxyepinephrine
DiastoleDiastole
KaliuresisKaliuresis
ProgesteroneProgesterone
OxytocinOxytocin
Calcium gluconateCalcium gluconate
Nephrogenic diabetes insipidusNephrogenic diabetes insipidus
16α-Hydroxyprogesterone16α-Hydroxyprogesterone
CD-NPCD-NP
Brain natriuretic peptideBrain natriuretic peptide
Dents diseaseDent's disease
Endothelin receptorEndothelin receptor
Liz MillerLiz Miller
Atrial natriuretic peptideAtrial natriuretic peptide
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPsychiatry and PsychologyPhenomena and Processes
NatriuresisDiuresisSodiumKidneyAtrial Natriuretic FactorRenal CirculationNatriuretic AgentsGlomerular Filtration RateBlood PressureFurosemideWater-Electrolyte BalanceAldosteroneAminohippuric AcidsDiureticsInulinKidney TubulesReninKidney MedullaAngiotensin II Type 2 Receptor BlockersSodium, DietaryAngiotensin IIIElectrolytesBendroflumethiazideKidney Tubules, ProximalBlood VolumeBufanolidesSodium ChloridePotassiumSodium Chloride, DietaryUrinationDenervationHypertensionVasopressinsUrineFenoldopamArginine VasopressinReceptor, Angiotensin, Type 2DogsSodium Chloride SymportersIsotonic SolutionsCyclic GMPRenin-Angiotensin SystemOsmolar ConcentrationFludrocortisoneUrodynamicsSaline Solution, HypertonicHyponatremiaSolute Carrier Family 12, Member 1Kallikrein-Kinin SystemKidney Tubules, DistalNephronsHemodynamicsNatriuretic PeptidesAngiotensin IIDehydrationReceptors, Atrial Natriuretic FactorRats, Sprague-DawleyKidney CortexKidney Function TestsLithiumDiet, Sodium-RestrictedHydrostatic PressureWater DeprivationSodium Chloride Symporter InhibitorsParabiosisRenal AgentsMeclofenamic AcidPuncturesThiorphanPolyuriaPlasma SubstitutesHypertension, RenalMelanocyte-Stimulating HormonesWater-Electrolyte ImbalanceSodium-Potassium-Exchanging ATPaseRenal ArteryAnesthesiaChlorothiazideNeprilysinOxytocinImidazolesMetoclopramideRegional Blood FlowPlasma VolumeRats, WistarKidney Tubules, CollectingPyridinesRats, Inbred SHRTetrazolesImmersionReceptors, Dopamine D1DihydroxyphenylalanineAngiotensin II Type 1 Receptor BlockersBenzimidazolesRats, Inbred StrainsDrinkingLoop of HenleCardenolidesMetolazoneExtracellular SpaceHematocritDopamineNG-Nitroarginine Methyl EsterEpithelial Sodium ChannelsRats, Inbred WKYSodium-Potassium-Chloride SymportersSodium-Phosphate Cotransporter Proteins, Type IIHypernatremiaReceptors, VasopressinNephrectomyDose-Response Relationship, DrugInjections, IntraventricularCreatinineSodium-Hydrogen AntiporterInappropriate ADH SyndromeImidazoline ReceptorsKidney Concentrating AbilityPerfusionp-Aminohippuric AcidInfusions, IntravenousDesoxycorticosteroneAntihypertensive AgentsDeamino Arginine VasopressinKininsPressureNitric OxideChloridesWaterAngiotensin-Converting Enzyme InhibitorsBenzazepinesRats, Mutant Strains2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepineKidney Pelvis
Natriuresis - WikipediaNatriuresis - Wikipedia
Mechanisms of Big Endothelin-1-Induced Diuresis and Natriuresis | HypertensionMechanisms of Big Endothelin-1-Induced Diuresis and Natriuresis | Hypertension
Abnormal pressure natriuresis. A cause or a consequence of hypertension? | HypertensionAbnormal pressure natriuresis. A cause or a consequence of hypertension? | Hypertension
Antihypertensive mechanism of diuretics based on pressure-natriuresis relationship.Antihypertensive mechanism of diuretics based on pressure-natriuresis relationship.
Mechanisms of Polyuria and Natriuresis in Paroxysmal Tachycardia | Clinical Science | Portland PressMechanisms of Polyuria and Natriuresis in Paroxysmal Tachycardia | Clinical Science | Portland Press
The Renin-Aldosterone System in Exaggerated Natriuresis of Essential Hypertension | Clinical Science | Portland PressThe Renin-Aldosterone System in Exaggerated Natriuresis of Essential Hypertension | Clinical Science | Portland Press
ASSA14-03-08 Gastrin and D1 Dopamine Receptor Interact to Induce Natriuresis and Diuresis | HeartASSA14-03-08 Gastrin and D1 Dopamine Receptor Interact to Induce Natriuresis and Diuresis | Heart
The Effect of Beta Adrenergic Blockade on the Exaggerated Natriuresis and Diuresis of Hypertensive Patients. | Annals of...The Effect of Beta Adrenergic Blockade on the Exaggerated Natriuresis and Diuresis of Hypertensive Patients. | Annals of...
Inability of indomethacin to modify hydrochlorothiazide diuresis and natriuresis by the chimpanzee kidney. | Journal of...Inability of indomethacin to modify hydrochlorothiazide diuresis and natriuresis by the chimpanzee kidney. | Journal of...
Atrial natriuretic peptide released by rapid ventricular pacing in dogs does not cause a natriuresis | Clinical ScienceAtrial natriuretic peptide released by rapid ventricular pacing in dogs does not cause a natriuresis | Clinical Science
Failure of Selected Endocrine Organ Ablation to Modify the Natriuresis of Blood Volume Expansion in the Dog | Clinical ScienceFailure of Selected Endocrine Organ Ablation to Modify the Natriuresis of Blood Volume Expansion in the Dog | Clinical Science
RePub, Erasmus University Repository: Role of Dietary K+ in Natriuresis, Blood Pressure Reduction, Cardiovascular Protection,...RePub, Erasmus University Repository: Role of Dietary K+ in Natriuresis, Blood Pressure Reduction, Cardiovascular Protection,...
Role of Kinins in the Control of Renal Papillary Blood Flow, Pressure Natriuresis, and Arterial Pressure | Circulation ResearchRole of Kinins in the Control of Renal Papillary Blood Flow, Pressure Natriuresis, and Arterial Pressure | Circulation Research
Blunted natriuresis to atrial natriuretic peptide in chronic sodium-retaining disorders. - Semantic ScholarBlunted natriuresis to atrial natriuretic peptide in chronic sodium-retaining disorders. - Semantic Scholar
Role of right and left atria in natriuresis and atrial natriuretic factor release during blood volume changes in the conscious...Role of right and left atria in natriuresis and atrial natriuretic factor release during blood volume changes in the conscious...
Get PDF - Reduction of nocturnal diuresis and natriuresis during treatment of obstructive sleep apnea (OSA) with nasal...Get PDF - Reduction of nocturnal diuresis and natriuresis during treatment of obstructive sleep apnea (OSA) with nasal...
Natriuresis during and early after cardiopulmonary bypass: Relationship to atrial natriuretic factor, aldosterone, and...Natriuresis during and early after cardiopulmonary bypass: Relationship to atrial natriuretic factor, aldosterone, and...
Abstract 557: Chronic Compound-21 Infusion Induces Natriuresis in Wild-Type Mice but not in AT2 Receptor-Null MiceAbstract 557: Chronic Compound-21 Infusion Induces Natriuresis in Wild-Type Mice but not in AT2 Receptor-Null Mice
Role of atrial natriuretic peptide in volume-expansion natriuresis<...Role of atrial natriuretic peptide in volume-expansion natriuresis<...
Lifelong angiotensin converting enzyme inhibition, pressure natriuresis, and renin angiotensin system gene expression in...Lifelong angiotensin converting enzyme inhibition, pressure natriuresis, and renin angiotensin system gene expression in...
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Hypoxanthine plus xanthine oxidase causes profound natriuresis without affecting renal blood flow autoregulationHypoxanthine plus xanthine oxidase causes profound natriuresis without affecting renal blood flow autoregulation
Importance of Pressure Natriuresis and Pressure Diuresis in Maintaining Body Sodium and Fluid BalanceImportance of Pressure Natriuresis and Pressure Diuresis in Maintaining Body Sodium and Fluid Balance
Altered Expression of Major Renal Na Transporters in Rats with Unilateral Ureteral Obstruction - NDI FoundationAltered Expression of Major Renal Na Transporters in Rats with Unilateral Ureteral Obstruction - NDI Foundation
Chronic taurine treatment ameliorates reduction in saline-induced diuresis and natriuresis<...Chronic taurine treatment ameliorates reduction in saline-induced diuresis and natriuresis<...
Interleukin-1 induces natriuresis in conscious rats: Role of renal prostaglandins<...Interleukin-1 induces natriuresis in conscious rats: Role of renal prostaglandins<...
April 1996 - Volume 14 - Issue 4 : Journal of HypertensionApril 1996 - Volume 14 - Issue 4 : Journal of Hypertension
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AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPsychiatry and PsychologyPhenomena and Processes
NatriuresisDiuresisSodiumKidneyAtrial Natriuretic FactorRenal CirculationNatriuretic AgentsGlomerular Filtration RateBlood PressureFurosemideWater-Electrolyte BalanceAldosteroneAminohippuric AcidsDiureticsInulinKidney TubulesReninKidney MedullaAngiotensin II Type 2 Receptor BlockersSodium, DietaryAngiotensin IIIElectrolytesBendroflumethiazideKidney Tubules, ProximalBlood VolumeBufanolidesSodium ChloridePotassiumSodium Chloride, DietaryUrinationDenervationHypertensionVasopressinsUrineFenoldopamArginine VasopressinReceptor, Angiotensin, Type 2DogsSodium Chloride SymportersIsotonic SolutionsCyclic GMPRenin-Angiotensin SystemOsmolar ConcentrationFludrocortisoneUrodynamicsSaline Solution, HypertonicHyponatremiaSolute Carrier Family 12, Member 1Kallikrein-Kinin SystemKidney Tubules, DistalNephronsHemodynamicsNatriuretic PeptidesAngiotensin IIDehydrationReceptors, Atrial Natriuretic FactorRats, Sprague-DawleyKidney CortexKidney Function TestsLithiumDiet, Sodium-RestrictedHydrostatic PressureWater DeprivationSodium Chloride Symporter InhibitorsParabiosisRenal AgentsMeclofenamic AcidPuncturesThiorphanPolyuriaPlasma SubstitutesHypertension, RenalMelanocyte-Stimulating HormonesWater-Electrolyte ImbalanceSodium-Potassium-Exchanging ATPaseRenal ArteryAnesthesiaChlorothiazideNeprilysinOxytocinImidazolesMetoclopramideRegional Blood FlowPlasma VolumeRats, WistarKidney Tubules, CollectingPyridinesRats, Inbred SHRTetrazolesImmersionReceptors, Dopamine D1DihydroxyphenylalanineAngiotensin II Type 1 Receptor BlockersBenzimidazolesRats, Inbred StrainsDrinkingLoop of HenleCardenolidesMetolazoneExtracellular SpaceHematocritDopamineNG-Nitroarginine Methyl EsterEpithelial Sodium ChannelsRats, Inbred WKYSodium-Potassium-Chloride SymportersSodium-Phosphate Cotransporter Proteins, Type IIHypernatremiaReceptors, VasopressinNephrectomyDose-Response Relationship, DrugInjections, IntraventricularCreatinineSodium-Hydrogen AntiporterInappropriate ADH SyndromeImidazoline ReceptorsKidney Concentrating AbilityPerfusionp-Aminohippuric AcidInfusions, IntravenousDesoxycorticosteroneAntihypertensive AgentsDeamino Arginine VasopressinKininsPressureNitric OxideChloridesWaterAngiotensin-Converting Enzyme InhibitorsBenzazepinesRats, Mutant Strains2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepineKidney Pelvis
Diuresis and NatriuresisInduced natriuresis and diuresisVasodilationAtrialExcretion of sodiumRatsArterial pressureInduce natriuresisUrineMechanismsInducesReninNatriureticBlockadeMedullaryStimulation of renalAngiotensinGlomerular filtPolyuriaCGMPRenal functionInfusionAbnormalReduction in bloodMechanismAcuteReceptorEffectsRelationshipOccurs
Diuresis and Natriuresis10
Induced natriuresis and diuresis1
Vasodilation2
Atrial7
Excretion of sodium3
Rats10
Arterial pressure3
Induce natriuresis1
Urine5
  • Natriuresis is the process of sodium excretion in the urine through the action of the kidneys. (wikipedia.org)
  • Natriuresis lowers the concentration of sodium in the blood and also tends to lower blood volume because osmotic forces drag water out of the body's blood circulation and into the urine along with the sodium. (wikipedia.org)
  • Urine collection for 2 h after release of UUO revealed a significant reduction in urinary osmolality , solute-free water reabsorption, and a marked natriuresis (0.29 +/- 0.03 vs. 0.17 +/- 0.03 micromol/min, P (ndif.org)
  • Our mouse renal clearance model confirms these results and shows significant natriuresis following a constant infusion of uroguanylin for 30 min, while the glomerular filtration rate, plasma creatinine, urine osmolality, heart rate, and blood pressure remain constant. (scielo.br)
  • 3. Kinin generated showed natriuresis through B_2 receptor localized on the luminal side of the tubular cells, as shown by increased natriuresis by ebelactone B,which selectively inhibited carboxypeptidase Y-like exopeptidase in urine. (nii.ac.jp)
Mechanisms3
Induces1
  • These data demonstrate that medullary NaCl loading induces ET-1 and P2-independent natriuresis in intact females. (bireme.br)
Renin1
Natriuretic2
  • 1. Selected organ-ablation experiments were performed in dogs in an attempt to identify the source of the natriuretic hormone postulated to participate in the natriuresis of blood volume expansion. (clinsci.org)
  • Pretreatment with the cyclooxygenease inhibitor, ibuprofen, signficantly attenuated the natriuretic response and indomethacin completely abolished the natriuresis. (elsevier.com)
Blockade2
Medullary3
Stimulation of renal2
Angiotensin3
  • Our previous studies have demonstrated that angiotensin (Ang) type-2 receptors (AT2R) mediate natriuresis by inhibiting Na+ reabsorption in the renal proximal tubule and that des1-aspartyl-Ang II (Ang III) is the preferred endogenous agonist for this response. (ovid.com)
  • This effect is independent of changes in activity of the sym-pathetic nervous system or of various hormones, such as angiotensin II, ADH, or aldosterone, because pres-sure natriuresis can be demonstrated in an isolated kidney that has been removed from the influence of these factors. (brainkart.com)
  • Angiotensin II natriuresis and anti-natriuresis: role of renal artery pressure in anaesthetized dogs. (biomedsearch.com)
Glomerular filt1
  • The natriuresis elicited by 3 μg hrIL-1 was independent of changes in glomerular filtration rate or effective renal plasma flow. (elsevier.com)
Polyuria1
  • The main features are polyuria, natriuresis and hyponatraemia secondary to disruption of hypothalamic and renal tracts . (bmj.com)
CGMP2
Renal function1
Infusion2
Abnormal1
Reduction in blood1
Mechanism1
  • Interestingly, GC-C knockout mice ( Gucy 2 c -/-) also exhibit significant uroguanylin-induced natriuresis and kaliuresis in vivo , suggesting the presence of an alternate receptor signaling mechanism in the kidney. (scielo.br)
Acute1
  • We propose that IL-1-induced natriuresis may be a component of the overall acute phase response which is actively mounted by the host during infection. (elsevier.com)
Receptor3
  • Natriuresis and diuresis was partially blocked by SCH23390 or CI988, indicating the interaction between gastrin and D1-like receptor. (bmj.com)
  • Peripheral and central imidazoline receptor-mediated natriuresis in the rat. (nih.gov)
  • Ovariectomy uncovers purinergic receptor activation of endothelin-dependent natriuresis. (bireme.br)
Effects1
  • The same general effects of natriuresis were observed for both irrigating solutions, although the volume of infused 1.5% glycine had a higher tendency to enter the intracellular fluid space. (scielo.br)
Relationship1
Occurs1
  • We conclude that the early natriuresis during CPB occurs in the presence of a high ADH concentration, with no significant increase in plasma α-ANF. (elsevier.com)

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