Sodium excretion by URINATION.
An increase in the excretion of URINE. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
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.
The circulation of the BLOOD through the vessels of the KIDNEY.
Endogenous or exogenous chemicals that regulate the WATER-ELECTROLYTE BALANCE in the body. They consist of peptides and non-peptide compounds.
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.
A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.
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.
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.
A group of glycine amides of aminobenzoic acids.
Agents that promote the excretion of urine through their effects on kidney function.
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.
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.
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
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.
Agents that antagonize the ANGIOTENSIN II TYPE 2 RECEPTOR.
Sodium or sodium compounds used in foods or as a food. The most frequently used compounds are sodium chloride or sodium glutamate.
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%).
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)
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)
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.
Volume of circulating BLOOD. It is the sum of the PLASMA VOLUME and ERYTHROCYTE VOLUME.
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.
A ubiquitous sodium salt that is commonly used to season food.
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 used in foods.
Discharge of URINE, liquid waste processed by the KIDNEY, from the body.
The resection or removal of the nerve to an organ or part. (Dorland, 28th ed)
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.
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.
Liquid by-product of excretion produced in the kidneys, temporarily stored in the bladder until discharge through the URETHRA.
A dopamine D1 receptor agonist that is used as an antihypertensive agent. It lowers blood pressure through arteriolar vasodilation.
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.
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.
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)
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.
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)
Guanosine cyclic 3',5'-(hydrogen phosphate). A guanine nucleotide containing one phosphate group which is esterified to the sugar moiety in both the 3'- and 5'-positions. It is a cellular regulatory agent and has been described as a second messenger. Its levels increase in response to a variety of hormones, including acetylcholine, insulin, and oxytocin and it has been found to activate specific protein kinases. (From Merck Index, 11th ed)
A 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.
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.
A synthetic mineralocorticoid with anti-inflammatory activity.
The mechanical laws of fluid dynamics as they apply to urine transport.
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).
Deficiency of sodium in the blood; salt depletion. (Dorland, 27th ed)
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.
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.
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.
The functional units of the kidney, consisting of the glomerulus and the attached tubule.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
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).
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
The condition that results from excessive loss of water from a living organism.
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.
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.
The outer zone of the KIDNEY, beneath the capsule, consisting of KIDNEY GLOMERULUS; KIDNEY TUBULES, DISTAL; and KIDNEY TUBULES, PROXIMAL.
Laboratory tests used to evaluate how well the kidneys are working through examination of blood and urine.
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.
A diet which contains very little sodium chloride. It is prescribed by some for hypertension and for edematous states. (Dorland, 27th ed)
The pressure due to the weight of fluid.
The withholding of water in a structured experimental situation.
Agents that inhibit SODIUM CHLORIDE SYMPORTERS. They act as DIURETICS. Excess use is associated with HYPOKALEMIA.
The experimental joining of two individuals for the purpose of studying the effects of one on the other.
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.
A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis.
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.
A potent inhibitor of membrane metalloendopeptidase (ENKEPHALINASE). Thiorphan potentiates morphine-induced ANALGESIA and attenuates naloxone-precipitated withdrawal symptoms.
Urination of a large volume of urine with an increase in urinary frequency, commonly seen in diabetes (DIABETES MELLITUS; DIABETES INSIPIDUS).
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.
Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.
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.
Disturbances in the body's WATER-ELECTROLYTE BALANCE.
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.
A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters.
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.
A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p812)
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.
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.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
A dopamine D2 antagonist that is used as an antiemetic.
The flow of BLOOD through or around an organ or region of the body.
Volume of PLASMA in the circulation. It is usually measured by INDICATOR DILUTION TECHNIQUES.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
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.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.
The placing of a body or a part thereof into a liquid.
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.
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.
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.
Compounds with a BENZENE fused to IMIDAZOLES.
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.
The consumption of liquids.
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.
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.
A quinazoline-sulfonamide derived DIURETIC that functions by inhibiting SODIUM CHLORIDE SYMPORTERS.
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.
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.
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.
A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
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.
A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).
A subclass of symporters that specifically transport SODIUM CHLORIDE and/or POTASSIUM CHLORIDE across cellular membranes in a tightly coupled process.
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.
Excessive amount of sodium in the blood. (Dorland, 27th ed)
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.
Excision of kidney.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Injections into the cerebral ventricles.
A plasma membrane exchange glycoprotein transporter that functions in intracellular pH regulation, cell volume regulation, and cellular response to many different hormones and mitogens.
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.
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.
The ability of the kidney to excrete in the urine high concentrations of solutes from the blood plasma.
Treatment process involving the injection of fluid into an organ or tissue.
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.
The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.
A steroid metabolite that is the 11-deoxy derivative of CORTICOSTERONE and the 21-hydroxy derivative of PROGESTERONE.
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.
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)
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)
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.
Inorganic compounds derived from hydrochloric acid that contain the Cl- ion.
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)
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.
Compounds with BENZENE fused to AZEPINES.
Rats bearing mutant genes which are phenotypically expressed in the animals.
A selective D1 dopamine receptor agonist used primarily as a research tool.
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)

There are two types of hypertension:

1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.

Some common causes of secondary hypertension include:

* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use

There are also several risk factors for hypertension, including:

* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress

Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:

* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease

Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.

Hyponatremia can be caused by various factors, such as excessive fluid intake, certain medications, kidney or liver disease, and hormonal imbalances. Symptoms may include headache, nausea, vomiting, fatigue, muscle weakness, and in severe cases, seizures or coma.

Treatment for hyponatremia typically involves correcting the underlying cause of the condition. This may involve discontinuing certain medications, addressing any underlying medical conditions, or limiting fluid intake. In severe cases, hospitalization may be necessary to monitor and treat the condition. In some instances, sodium supplements or diuretics may be prescribed to help correct sodium levels.

It is important to note that hyponatremia can be a serious condition, and prompt medical attention should be sought if symptoms persist or worsen over time. A healthcare professional should be consulted for proper diagnosis and treatment.

There are many potential causes of dehydration, including:

* Not drinking enough fluids
* Diarrhea or vomiting
* Sweating excessively
* Diabetes (when the body cannot properly regulate blood sugar levels)
* Certain medications
* Poor nutrition
* Infections
* Poor sleep

To diagnose dehydration, a healthcare provider will typically perform a physical examination and ask questions about the patient's symptoms and medical history. They may also order blood tests or other diagnostic tests to rule out other conditions that may be causing the symptoms.

Treatment for dehydration usually involves drinking plenty of fluids, such as water or electrolyte-rich drinks like sports drinks. In severe cases, intravenous fluids may be necessary. If the underlying cause of the dehydration is a medical condition, such as diabetes or an infection, treatment will focus on managing that condition.

Preventing dehydration is important for maintaining good health. This can be done by:

* Drinking enough fluids throughout the day
* Avoiding caffeine and alcohol, which can act as diuretics and increase urine production
* Eating a balanced diet that includes plenty of fruits, vegetables, and whole grains
* Avoiding excessive sweating by dressing appropriately for the weather and taking breaks in cool, shaded areas when necessary
* Managing medical conditions like diabetes and kidney disease properly.

In severe cases of dehydration, complications can include seizures, organ failure, and even death. It is important to seek medical attention if symptoms persist or worsen over time.

In diabetes, polyuria is caused by high levels of glucose in the blood that cannot be properly absorbed by the body. The excess glucose spills into the urine, drawing water with it and increasing the volume of urine. This can lead to dehydration and electrolyte imbalances if left untreated.

In kidney disease, polyuria can be caused by damage to the kidneys that impairs their ability to concentrate urine. As a result, the body produces more urine than usual to compensate for the lack of concentrating ability.

Polyuria can also be a symptom of certain endocrine disorders such as diabetes insipidus, where the body produces too much antidiuretic hormone (ADH) or vasopressin, which leads to an excessive amount of urine production.

To diagnose polyuria, a healthcare provider may perform a physical examination, take a medical history, and conduct diagnostic tests such as urinalysis, blood glucose testing, and imaging studies. Treatment for polyuria depends on the underlying cause and may include medication, lifestyle changes, and in some cases, dialysis.

A type of hypertension that is caused by a problem with the kidneys. It can be acute or chronic and may be associated with other conditions such as glomerulonephritis, pyelonephritis, or polycystic kidney disease. Symptoms include proteinuria, hematuria, and elevated blood pressure. Treatment options include diuretics, ACE inhibitors, and angiotensin II receptor blockers.

Note: Renal hypertension is also known as renal artery hypertension.

Water-electrolyte imbalance can be caused by various factors such as excessive sweating, diarrhea, vomiting, burns, and certain medications. It can also be a complication of other medical conditions like kidney disease, heart failure, and liver disease.

Symptoms of water-electrolyte imbalance may include:

* Dehydration or overhydration
* Changes in blood pH (acidosis or alkalosis)
* Electrolyte abnormalities (such as low sodium, high potassium, or low bicarbonate)
* Muscle weakness or cramping
* Confusion or disorientation
* Heart arrhythmias

Treatment of water-electrolyte imbalance depends on the underlying cause and the severity of symptoms. Fluid replacement, electrolyte supplements, and medications to correct pH levels may be prescribed by a healthcare professional. In severe cases, hospitalization may be necessary to monitor and treat the condition.

It is important to seek medical attention if you experience any symptoms of water-electrolyte imbalance, as untreated imbalances can lead to serious complications such as seizures, coma, and even death.

Hypernatremia can cause a range of symptoms including headache, nausea, vomiting, confusion, and in severe cases, seizures and coma. Treatment for hypernatremia typically involves correcting the underlying cause and fluid and electrolyte replacement therapy to restore normal sodium levels in the blood. In severe cases, hospitalization may be required to monitor and treat the condition closely.

It is important to note that hypernatremia can have serious complications if left untreated or if treated too late, such as seizures, coma, and even death. Therefore, prompt medical attention is essential if symptoms persist or worsen over time.

A more detailed explanation of Inappropriate ADH Syndrome may be as follows:

Inappropriate ADH syndrome is a rare endocrine disorder characterized by excessive antidiuretic hormone (ADH) secretion, leading to water retention and hyponatremia. Hyponatremia occurs when the body contains too much water and not enough sodium, causing an imbalance in the electrolyte levels of the blood. This condition can be caused by various factors such as a tumor or other abnormality that increases ADH production or decreases sodium levels in the body. Symptoms of Inappropriate ADH syndrome may include headaches, nausea, vomiting, seizures, and in severe cases, coma.

If left untreated, Inappropriate ADH Syndrome can lead to more serious complications such as seizures or coma. Treatment options for this condition typically involve surgery, radiation therapy, or medication to remove the tumor or other abnormality causing the excessive ADH production and restore sodium levels in the body. It is important to seek medical attention if symptoms persist or worsen over time as early diagnosis and treatment can improve the chances of a successful outcome for this condition.

In summary, Inappropriate ADH Syndrome is an uncommon endocrine disorder caused by excessive ADH secretion leading to hyponatremia due to water retention, which can cause severe symptoms such as headache, nausea, vomiting, seizures, and coma if left untreated. Treatment options involve surgery, radiation therapy, or medication to remove the tumor or other abnormality causing excessive ADH production and restore sodium levels in the body. Early diagnosis and treatment are crucial for a successful outcome.

... is the process of sodium excretion in the urine through the action of the kidneys. It is promoted by ventricular ... Natriuresis lowers the concentration of sodium in the blood and also tends to lower blood volume because osmotic forces drag ... Excess natriuresis can be caused by: Medullary cystic disease Bartter syndrome Diuretic phase of acute tubular necrosis Some ... "Natriuresis". Merriam-Webster. Retrieved 23 December 2013. Boron, Walter F. and Boulpaep, Emile L. "Medical Physiology". ...
Dopamine signaling affects diuresis and natriuresis. Dysfunction of dopaminergic neurotransmission in the CNS has been ...
Nesiritide promotes diuresis and natriuresis, thereby ameliorating volume overload. It is thought that, while BNP is elevated ...
Normalization of arterial pressure after barodenervation: role of pressure natriuresis. Am J Physiol. 1990;259(6 Pt 2):R1172- ... role of pressure natriuresis". The American Journal of Physiology. 259 (6 Pt 2): R1172-1180. doi:10.1152/ajpregu.1990.259.6. ...
... and lead to increased natriuresis (excretion of sodium in the urine). Renin increases in concentration in the blood as a result ...
McDonough AA, Leong PK, Yang LE (2003). "Mechanisms of pressure natriuresis: how blood pressure regulates renal sodium ...
In doing so, ARBs block vasoconstriction, promote natriuresis, and reduce oxidative stress. Studies show that the vasodilator ... increase natriuresis, decrease blood volume, all of which culminate in lowering blood pressure. Enalapril, Benazepril, ...
NPs provide natriuresis, diuresis, vasodilation, antiproliferation, antihypertrophy, antifibrosis and other cardiometabolic ...
Spahr L, Villeneuve JP, Tran HK, Pomier-Layrargues G (2001). "Furosemide-induced natriuresis as a test to identify cirrhotic ...
It also appears to exacerbate proteinuria and natriuresis in patients with nephrotic syndrome. Engleback, I. M.; Lappe, R. W.; ...
... (URO) is a hormone that causes natriuresis by increasing renal blood flow. It is secreted in response to increased ... When administered intravenously, urodilatin induces strong diuresis and natriuresis with tolerable hemodynamic side effects. ... which induces diuresis and natriuresis, differentially processed to a peptide of 32 amino acids from the same precursor as ...
In the kidney, it is inhibited by atrial natriuretic peptide, causing natriuresis and diuresis. Epithelial Na+ channels (ENaCs ...
Matthiesen, TB; Rittig, S; Nørgaard, JP; Pedersen, EB; Djurhuus, JC (1996). "Nocturnal polyuria and natriuresis in male ...
Natriuresis Harrison's Principles of Internal Medicine, 16th edition Merriam-Webster entry Welling, Paul A. (2013). "Regulation ...
It is localized in the kidney where it results in natriuresis upon binding to natriuretic peptides. However, it is found in ...
A natriuretic peptide is a peptide that induces natriuresis, which is the excretion of sodium by the kidneys. Known natriuretic ...
This increase is due to both a diuresis (increase in water excretion) and a natriuresis (increase in saline excretion); it is ...
... promoting natriuresis, diuresis, vasodilation, and reductions in preload and ventricular remodeling. It was discovered and ...
The resulting natriuresis is of lesser magnitude than the water diuresis, leading eventually to excessive water loss and ...
The ANP causes increased natriuresis, while the hypothalamus, in turn, decreases the production of vasopressin (ADH, AVP, or ...
Both drugs increased diuresis and natriuresis - effects that are thought to be due to the activation of renal D1 receptors. It ...
Elevated levels of BNP indicate excessive natriuresis (excretion of sodium to the urine) and decline of ventricular function, ...
"Blood pressure reduction by Japanese traditional Miso is associated with increased diuresis and natriuresis through dopamine ...
... natriuresis). Giving chlortalidone while simultaneously restricting dietary sodium intake causes mild hypovolemia (low ...
Elevated levels of progesterone potently reduce the sodium-retaining activity of aldosterone, resulting in natriuresis and a ... Progesterone withdrawal, on the other hand, is associated with a temporary increase in sodium retention (reduced natriuresis, ... such as natriuresis, at physiological concentrations. In addition, progesterone binds to and behaves as a partial agonist of ...
In several species, oxytocin can stimulate sodium excretion from the kidneys (natriuresis), and, in humans, high doses can ...
High blood calcium causes natriuresis (increased sodium loss in the urine) and water diuresis, in part by its effect through ...
It was found to produce natriuresis similar to that produced by spironolactone when administered to humans, suggesting that it ...
... was the only drug in the screen that was capable of causing the excretion of sodium (natriuresis) without a ...
... through natriuresis/diuresis) and inhibition of pro-fibrotic, remodeling pathways. McKie PM, Sangaralingham SJ, Burnett JC ( ...
Acute and chronic effects of captopril on the renin-angiotensin and kallikrein systems affecting blood pressure and natriuresis ...
Home Studies Heart Failure Network (HFN) Aldosterone Targeted Neurohormonal Combined with Natriuresis Therapy - HF (ATHENA HF) ... Heart Failure Network (HFN) Aldosterone Targeted Neurohormonal Combined with Natriuresis Therapy - HF (ATHENA HF) ...
... chloride loading is pressor in the stroke-prone spontaneously hypertensive rat despite hydrochlorothiazide-induced natriuresis ...
Natriuresis. 1. 1991. 124. 0.030. Why? Cholangiopancreatography, Endoscopic Retrograde. 1. 2014. 488. 0.030. Why? ...
Natriuresis causes a secondary loss of potassium.. Pharmacokinetics and Metabolism. Bisoprolol and hydrochlorothiazide. In ...
The collecting duct is the predominant nephron site of prorenin and prorenin receptor (PRR) expression. We previously demonstrated that the collecting duct PRR regulates epithelial Na|sup|+|/sup| channel (ENaC) activity and water transport; however, which cell type is involved remains unclear. Herei …
... their role in the molecular physiology of pressure-natriuresis; new animal models of transport dysregulation for genetic as ...
GLP-1 has other effects too, like natriuresis, diuresis, BP reduction and reducing of inflammation. Diabetes trials have found ...
Evidence indicating that this anomaly in the pressure natriuresis relationship arises from a sympathetic nervous system ... The renal-mean arterial pressure set-point model is briefly described to explain that a shift of the pressure natriuresis ... Natriuresis is itself determined by the kidneys perfusion pressure, therefore the application of the pressure-natriuresis ... A key component of this feedback is the pressure natriuresis or the effect of arterial pressure on renal sodium and water ...
Natriuresis may be accompanied by some loss of potassium and bicarbonate.. After oral use diuresis begins within 2 hours, peaks ...
The acute pressure natriuresis response is suppressed by selective ETA receptor blockade Geoffrey Culshaw; David Binnie; Neeraj ... View articletitled, The acute pressure natriuresis response is suppressed by selective ET,sub,A,/sub, receptor blockade ...
Blunted pressure natriuresis in the Brattleboro diabetes insipidus rat. Gonzalez-Campoy, J.M., Awazu, M., Granger, J.P., Haas, ... as evidenced by an increase in water consumption to approximately four times normal completely abolished the natriuresis and ...
Natriuresis Preferred Concept UI. M0014511. Scope Note. Sodium excretion by URINATION.. Terms. Natriuresis Preferred Term Term ... differentiate from SODIUM /‌urine in that in natriuresis emphasis is on the physiological process of urinary excretion of ... Natriuresis. Tree Number(s). G08.852.179.557. Unique ID. D009318. RDF Unique Identifier. ...
Volume-induced natriuresis in healthy women: renal metabolism of prostacyclin and thromboxane, and physiological role of ...
... has long been shown that treatment with a combination of thiazide and NSAID initially reduces polyuria and promotes natriuresis ...
No Need to Sugarcoat the Message: Is Cardiovascular Risk Reduction From SGLT2 Inhibition Related to Natriuresis? Perkins BA, ...
TY - JOUR. T1 - Chorioretinal thinning in chronic kidney disease links to inflammation and endothelial dysfunction. AU - Balmforth, Craig. AU - van Bragt, Job J.M.H. AU - Ruijs, Titia. AU - Cameron, James. AU - Kimmitt, Robert A.. AU - Moorhouse, Rebecca. AU - Czopek, Alicja. AU - Khei, Hu May. AU - Gallacher, Peter James. AU - Dear, James. AU - Borooah, Shyamanga. AU - MacIntyre, Iain. AU - Pearson, Tom MC. AU - Willox, Laura AU - Talwar, Dinesh. AU - Tafflet, Muriel. AU - Roubeix, Christophe. AU - Sennlaub, Florian AU - Chandran, Siddharthan. AU - Dhillon, Baljean. AU - Webb, David J AU - Dhaun, Neeraj. PY - 2016/12/8. Y1 - 2016/12/8. N2 - BACKGROUND. Chronic kidney disease (CKD) is strongly associated with cardiovascular disease and there is an established association between vasculopathy affecting the kidney and eye. Optical coherence tomography (OCT) is a novel, rapid method for high-definition imaging of the retina and choroid. Its use in patients at high cardiovascular disease risk ...
Hypertensive animal models respond to diltiazem with reductions in blood pressure and increased urinary output and natriuresis ...
... pressure-natriuresis mechanisms, role of interstitial hydrostatic pressure in volume regulation ...
... natriuresis, cell survival, and cell adhesion. After treatment with epidermal growth factor or ouabain, epithelial dog kidney ...
You will find known if DepoProvera natriuresis and may have undesirable effects a small increase to avoid possible. Some men ...
... natriuresis and diuresis [70-72]. Like BNP it is released in proportion to the severity of heart failure [73, 74], and is ... natriuresis and diuresis [61]. Endothelin appears to be detrimental post-MI, extending the infarct [62] and reducing coronary ... central venous pressure and natriuresis. BNP has been studied extensively and provides prognostic information following an MI [ ...
Effect of γ-tocopherol supplementation on premenstrual symptoms and natriuresis: a randomized, double-blind, placebo-controlled ...
Diuresis without natriuresis. The post-peak and late phases of diuresis in Aedes are characterised by the excretion of K+-rich ... Natriuresis also requires the activation of a cyclic-AMP-dependent bumetanide-sensitive Na+/K+/2Cl-cotransporter in the basal ... The shift from natriuresis to kaliuresis suggests that primary urine production is no longer stimulated by MNP (i.e. Anoga-DH31 ... Rather, the peak phase of diuresis and its associated natriuresis are attributed to the release of a peptide diuretic hormone ( ...
differentiate from SODIUM /urine in that in natriuresis emphasis is on the physiological process of urinary excretion of sodium ...
Natriuresis G8.852.796.241.557 G8.852.179.557 Natriuretic Peptide, Brain D12.776.641.590 D12.776.631.590 Natural Childbirth ...
Natriuresis Preferred Concept UI. M0014511. Scope Note. Sodium excretion by URINATION.. Terms. Natriuresis Preferred Term Term ... differentiate from SODIUM /‌urine in that in natriuresis emphasis is on the physiological process of urinary excretion of ... Natriuresis. Tree Number(s). G08.852.179.557. Unique ID. D009318. RDF Unique Identifier. ...
  • Additionally, the actions of both BNP and ANP result in a decrease in cardiac output due to an overall decrease in central venous pressure and preload as a result of the reduction in blood volume that follows natriuresis and diuresis. (
  • Among the numerous metabolic effects of GLP-1 are the glucose-dependent stimulation of insulin secretion, decrease of gastric emptying, inhibition of food intake, increase of natriuresis and diuresis, and modulation of rodent β-cell proliferation. (
  • This natriuresis and diuresis is accompanied by a secondary loss of potassium and bicarbonate. (
  • They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility. (
  • The kidneys also control sodium excretion through a process called pressure natriuresis. (
  • This "natriuresis of fasting" can cause sodium deficiency and lead to unpleasant symptoms like muscle cramps, headaches, and fatigue. (
  • EGF is regarded as the main protector against injuries in epithelia, and ouabain is a hormone that regulates blood pressure, natriuresis, cell survival, and cell adhesion. (
  • The physiologic actions of BNP are similar to those of ANP and include decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis . (
  • You will find known if DepoProvera natriuresis and may have undesirable effects a small increase to avoid possible. (
  • Natriuresis levels did not differ by sex. (