Diuresis
Sodium
Kidney
Atrial Natriuretic Factor
Natriuretic Agents
Glomerular Filtration Rate
Furosemide
Water-Electrolyte Balance
Aldosterone
Inulin
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
Kidney Medulla
Sodium, Dietary
Angiotensin III
Electrolytes
Bendroflumethiazide
Kidney Tubules, Proximal
Bufanolides
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.
Hypertension
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
Fenoldopam
Arginine Vasopressin
Receptor, Angiotensin, Type 2
Dogs
Sodium Chloride Symporters
Isotonic Solutions
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
Saline Solution, Hypertonic
Solute Carrier Family 12, Member 1
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
Hemodynamics
Natriuretic Peptides
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.
Receptors, Atrial Natriuretic Factor
Rats, Sprague-Dawley
Kidney Cortex
Kidney Function Tests
Lithium
Diet, Sodium-Restricted
Sodium Chloride Symporter Inhibitors
Parabiosis
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
Punctures
Thiorphan
Polyuria
Plasma Substitutes
Hypertension, Renal
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.
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.
Anesthesia
Chlorothiazide
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
Imidazoles
Plasma Volume
Rats, Wistar
Kidney Tubules, Collecting
Pyridines
Rats, Inbred SHR
Receptors, Dopamine D1
Dihydroxyphenylalanine
Angiotensin II Type 1 Receptor Blockers
Rats, Inbred Strains
Loop of Henle
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
Extracellular Space
Hematocrit
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
Epithelial Sodium Channels
Rats, Inbred WKY
Sodium-Potassium-Chloride Symporters
Sodium-Phosphate Cotransporter Proteins, Type II
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.
Dose-Response Relationship, Drug
Sodium-Hydrogen Antiporter
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
Kidney Concentrating Ability
p-Aminohippuric Acid
Infusions, Intravenous
Desoxycorticosterone
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
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
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.
Water
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.
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine
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)
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Fena Detergent Powder (Fena 500g) - Deshimall
Managing COPD: Medicines for Long-Term Control
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Can the generic form of Prilosec affect the prostate? Reduce urine flow?
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Dopamine receptor
Dopamine signaling affects diuresis and natriuresis. Dysfunction of dopaminergic neurotransmission in the CNS has been ...
Sarah K. England
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. ...
Sodium-hydrogen antiporter 3
McDonough AA, Leong PK, Yang LE (2003). "Mechanisms of pressure natriuresis: how blood pressure regulates renal sodium ...
Baroreflex
NPs provide natriuresis, diuresis, vasodilation, antiproliferation, antihypertrophy, antifibrosis and other cardiometabolic ...
Ascites
Spahr L, Villeneuve JP, Tran HK, Pomier-Layrargues G (2001). "Furosemide-induced natriuresis as a test to identify cirrhotic ...
Urodilatin
... (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 ...
Epithelial sodium channel
In the kidney, it is inhibited by atrial natriuretic peptide, causing natriuresis and diuresis. Epithelial Na+ channels (ENaCs ...
Nocturia
Matthiesen, TB; Rittig, S; Nørgaard, JP; Pedersen, EB; Djurhuus, JC (1996). "Nocturnal polyuria and natriuresis in male ...
Kaliuresis
Natriuresis Harrison's Principles of Internal Medicine, 16th edition Merriam-Webster entry Welling, Paul A. (2013). "Regulation ...
NPR1
It is localized in the kidney where it results in natriuresis upon binding to natriuretic peptides. However, it is found in ...
Natriuretic peptide
A natriuretic peptide is a peptide that induces natriuresis, which is the excretion of sodium by the kidneys. Known natriuretic ...
Omapatrilat
... promoting natriuresis, diuresis, vasodilation, and reductions in preload and ventricular remodeling. It was discovered and ...
Osmotic diuretic
The resulting natriuresis is of lesser magnitude than the water diuresis, leading eventually to excessive water loss and ...
ACE inhibitor
... and lead to increased natriuresis (excretion of sodium in the urine). Renin increases in concentration in the blood as a result ...
Progesterone
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 ...
Oxytocin
In several species, oxytocin can stimulate sodium excretion from the kidneys (natriuresis), and, in humans, high doses can ...
Dapagliflozin
... where SGLT2 inhibitors potently reduce intravascular volume through osmotic diuresis and natriuresis. This consequently may ...
16α-Hydroxyprogesterone
It was found to produce natriuresis similar to that produced by spironolactone when administered to humans, suggesting that it ...
Amiloride
... was the only drug in the screen that was capable of causing the excretion of sodium (natriuresis) without a ...
Cenderitide
... through natriuresis/diuresis) and inhibition of pro-fibrotic, remodeling pathways. McKie PM, Sangaralingham SJ, Burnett JC ( ...
Ventricular natriuretic peptide
... of ANP and include decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis. ... overall decrease in central venous pressure and preload as a result of the reduction in blood volume that follows natriuresis ...
Drospirenone
Due to its antimineralocorticoid activity, drospirenone increases natriuresis, decreases water retention and blood pressure, ...
Dent's disease
The impairment of Na transport in the distal convoluted tubule induces natriuresis and water loss, while increasing the ...
Pharmacodynamics of progesterone
Progesterone produces antimineralocorticoid effects such as natriuresis (excretion of sodium in the urine) at normal ...
Endothelin receptor
... natriuresis and diuresis (the production and elimination of urine) and mechanisms that lower blood pressure. ETB2 mediates ...
Liz Miller
"The Hypothalamic Control of sodium metabolism and the Syndrome of Inappropriate Natriuresis". The stress of her career, being ...
Atrial natriuretic peptide
... natriuresis) in the following ways: The medullary collecting duct is the main site of ANP regulation of sodium excretion. ANP ...
Aldosterone escape
... manifested by volume and/or pressure natriuresis. The inability of ACE inhibitor therapy to reliably suppress aldosterone ...
SGLT2 inhibitor
Pleiotropic effects of this class have been attributed to a variety of its pharmacodynamic actions such as natriuresis, ...
Arthur Guyton
... renal-pressure natriuresis, and long-term blood pressure regulation. The Textbook Memoriam continues: "Indeed, his concepts of ...
Natriuresis - Wikipedia
Natriuresis 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". ...
Mechanisms of Big Endothelin-1-Induced Diuresis and Natriuresis | Hypertension
Blockade of pressure natriuresis induced by inhibition of renal synthesis of nitric oxide in dogs. Am J Physiol. 1992;262:F718- ... Mechanisms of Big Endothelin-1-Induced Diuresis and Natriuresis. Role of ETB Receptors. Aaron Hoffman, Zaid A. Abassi, Sergey ... Hence, a pressure-natriuresis response due to big ET-1 activation of ETA receptors during ETB blockade cannot be excluded. ... Mechanisms of Big Endothelin-1-Induced Diuresis and Natriuresis. Aaron Hoffman, Zaid A. Abassi, Sergey Brodsky, Rawi Ramadan ...
Mechanisms of Polyuria and Natriuresis in Paroxysmal Tachycardia | Clinical Science | Portland Press
The Renin-Aldosterone System in Exaggerated Natriuresis of Essential Hypertension | Clinical Science | Portland Press
The Renin-Aldosterone System in Exaggerated Natriuresis of Essential Hypertension E. B. Pedersen E. B. Pedersen ... E. B. Pedersen, H. J. Kornerup; The Renin-Aldosterone System in Exaggerated Natriuresis of Essential Hypertension. Clin Sci Mol ... in plasma aldosterone concentration induced by sodium loading might be involved in the regulation of exaggerated natriuresis in ...
Diuresis and Natriuresis Caused by Activation of VR1-Positive Sensory Nerves in Renal Pelvis of Rats | Hypertension
Diuresis and Natriuresis Caused by Activation of VR1-Positive Sensory Nerves in Renal Pelvis of Rats. Yi Zhu, Youping Wang, ... Diuresis and Natriuresis Caused by Activation of VR1-Positive Sensory Nerves in Renal Pelvis of Rats ... Diuresis and Natriuresis Caused by Activation of VR1-Positive Sensory Nerves in Renal Pelvis of Rats ... Diuresis and Natriuresis Caused by Activation of VR1-Positive Sensory Nerves in Renal Pelvis of Rats ...
ASSA14-03-08 Gastrin and D1 Dopamine Receptor Interact to Induce Natriuresis and Diuresis | Heart
Natriuresis and diuresis was partially blocked by SCH23390 or CI988, indicating the interaction between gastrin and D1-like ... Result Gastrin infusing WKY rats via renal artery induced natriuresis and diuresis, which was blocked in the presence of CI988 ... Lower dosages of gastrin or fenoldopam failed to induce natriuresis and diuresis alone, while putting together induced the ... Objective Oral NaCl intake produces stronger natriuresis and diuresis than venous infusion of same amount, indicating the ...
The Effect of Beta Adrenergic Blockade on the Exaggerated Natriuresis and Diuresis of Hypertensive Patients. | Annals of...
The exaggerated natriuresis and diuresis of hypertensive patients to a hypertonic saline infusion was investigated to determine ... The Effect of Beta Adrenergic Blockade on the Exaggerated Natriuresis and Diuresis of Hypertensive Patients. William J. Mroczek ... The Effect of Beta Adrenergic Blockade on the Exaggerated Natriuresis and Diuresis of Hypertensive Patients.. Ann Intern Med. ; ...
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.. G M Fanelli, D L ... Inability of indomethacin to modify hydrochlorothiazide diuresis and natriuresis by the chimpanzee kidney.. G M Fanelli, D L ... Inability of indomethacin to modify hydrochlorothiazide diuresis and natriuresis by the chimpanzee kidney.. G M Fanelli, D L ... Inability of indomethacin to modify hydrochlorothiazide diuresis and natriuresis by the chimpanzee kidney. ...
Atrial natriuretic peptide released by rapid ventricular pacing in dogs does not cause a natriuresis | Clinical Science
Atrial natriuretic peptide released by rapid ventricular pacing in dogs does not cause a natriuresis. K. P. Walsh, T. D. M. ... Atrial natriuretic peptide released by rapid ventricular pacing in dogs does not cause a natriuresis ... Atrial natriuretic peptide released by rapid ventricular pacing in dogs does not cause a natriuresis ... Atrial natriuretic peptide released by rapid ventricular pacing in dogs does not cause a natriuresis ...
Failure of Selected Endocrine Organ Ablation to Modify the Natriuresis of Blood Volume Expansion in the Dog | Clinical Science
Failure of Selected Endocrine Organ Ablation to Modify the Natriuresis of Blood Volume Expansion in the Dog. G. J. Kaloyanides ... The natriuresis was unrelated to changes in glomerular filtration rate, renal blood flow, renal arterial pressure, plasma ... Failure of Selected Endocrine Organ Ablation to Modify the Natriuresis of Blood Volume Expansion in the Dog ... Failure of Selected Endocrine Organ Ablation to Modify the Natriuresis of Blood Volume Expansion in the Dog ...
Role of Kinins in the Control of Renal Papillary Blood Flow, Pressure Natriuresis, and Arterial Pressure | Circulation Research
8 A role for NO in pressure natriuresis is likely because NO synthesis blockade blunts pressure natriuresis and improves ... The dose of NAME (37 nmol · kg−1 · min−1 IV) was the minimum that blunted pressure natriuresis.9 The finding that there was no ... Role of Kinins in the Control of Renal Papillary Blood Flow, Pressure Natriuresis, and Arterial Pressure. Jerónimo Tornel, ... To examine the effects of Hoe140 on pressure natriuresis9 and the role of NO, vehicle (group 7), NAME (groups 8 and 10), or ...
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 ... 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 ... 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...
Reduction of nocturnal diuresis and natriuresis during treatment of obstructive sleep apnea (OSA) with nasal continuous ... Diurnal and nocturnal diuresis and natriuresis in obstructive sleep apnea. Effects of nasal continuous positive airway pressure ... Natriuresis and diuresis decreased by about 50% while creatinine excretion rate and urinary osmolality did not change. We found ... The decrease of diuresis, natriuresis and cGMP excretion demonstrate the beneficial effects of nCPAP treatment on the ...
Natriuresis during and early after cardiopulmonary bypass: Relationship to atrial natriuretic factor, aldosterone, and...
Schaff, H. V., Mashburn, J. P., McCarthy, P. M., Torres, E. J., Burnett, J. C., & Gannon (1989). Natriuresis during and early ... The natriuresis after CPB appears to be strongly associated with increased α-ANF, present for at least the first 30 minutes ... The natriuresis after CPB appears to be strongly associated with increased α-ANF, present for at least the first 30 minutes ... The natriuresis after CPB appears to be strongly associated with increased α-ANF, present for at least the first 30 minutes ...
Abstract 557: Chronic Compound-21 Infusion Induces Natriuresis in Wild-Type Mice but not in AT2 Receptor-Null Mice
Abstract 557: Chronic Compound-21 Infusion Induces Natriuresis in Wild-Type Mice but not in AT2 Receptor-Null Mice ... Our previous studies have demonstrated that angiotensin (Ang) type-2 receptors (AT2R) mediate natriuresis by inhibiting Na+ ... administered chronically in the absence of concurrent AT1R blockade can induce natriuresis in wild-type mice (WT; C57B6) and ...
Role of atrial natriuretic peptide in volume-expansion natriuresis<...
Role of atrial natriuretic peptide in volume-expansion natriuresis. T. R. Schwab, Brooks Sayre Edwards, D. M. Heublein, John C ... Role of atrial natriuretic peptide in volume-expansion natriuresis. / Schwab, T. R.; Edwards, Brooks Sayre; Heublein, D. M.; ... Schwab, TR, Edwards, BS, Heublein, DM & Burnett, JCJ 1986, Role of atrial natriuretic peptide in volume-expansion natriuresis ... Role of atrial natriuretic peptide in volume-expansion natriuresis. American Journal of Physiology - Regulatory Integrative and ...
Frontiers | GLP-1 Receptor Agonists in Diabetic Kidney Disease: From Clinical Outcomes to Mechanisms | Pharmacology
... which are mediated by natriuresis, anti-inflammatory and anti-oxidative stress properties. Recent clinical trials have ... which are mediated by natriuresis, anti-inflammatory and anti-oxidative stress properties. Furthermore, GLP-1RAs have been ... Natriuresis. Acute infusion of GLP-1 has been shown to stimulate diuresis and natriuresis in both experimental (Crajoinas et al ... cardiomyocyte GLP-1R plays an important role in natriuresis. It has been shown that liraglutide promotes natriuresis by atrial ...
Prouroguanylin, and Synthetic Analogs or Proteolytic Cleavage Products Derived from It, as Therepeutic and Diagnostic Agents...
Diuresis and Natriuresis Induced by Infused ProUGn. Native proUGn is purified from rat small intestine. Animals are sacrificed ... The decrease in natriuresis in the immunoblocked animals provides further evidence that proUGn (or one of its renal metabolites ... The term "postprandial natriuresis" is used to describe the entire renal natriuretic response to orogastric salt intake. The ... Suppl., 67, S242-S244 (1998). In recent years, a case also has been made for the direct mechanism, in which natriuresis is ...
Lifelong angiotensin converting enzyme inhibition, pressure natriuresis, and renin angiotensin system gene expression in...
Hypoxanthine plus xanthine oxidase causes profound natriuresis without affecting renal blood flow autoregulation
1995 - Volume 26 - Issue : Journal of Cardiovascular Pharmacology
Altered Expression of Major Renal Na Transporters in Rats with Unilateral Ureteral Obstruction - NDI Foundation
... to clarify the molecular mechanisms of the marked natriuresis seen after release of UUO. 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 ... major renal Na transporters in rats with UUO may contribute to the impairment in urinary concentrating capacity and natriuresis ... major renal Na transporters in rats with UUO may contribute to the impairment in urinary concentrating capacity and natriuresis ...
Chronic taurine treatment ameliorates reduction in saline-induced diuresis and natriuresis<...
Chronic taurine treatment ameliorates reduction in saline-induced diuresis and natriuresis. Mahmood S. Mozaffari, Stephen W. ... Chronic taurine treatment ameliorates reduction in saline-induced diuresis and natriuresis. / Mozaffari, Mahmood S.; Schaffer, ... Chronic taurine treatment ameliorated the reduction in saline-induced diuresis and natriuresis by both the UNX control and the ... Chronic taurine treatment ameliorated the reduction in saline-induced diuresis and natriuresis by both the UNX control and the ...
Interleukin-1 induces natriuresis in conscious rats: Role of renal prostaglandins<...
Interleukin-1 induces natriuresis in conscious rats: Role of renal prostaglandins. Kidney International. 1988 Jan 1;33(6):1059- ... Interleukin-1 induces natriuresis in conscious rats : Role of renal prostaglandins. / Beasley, D.; Dinarello, C. A.; Cannon, J ... The natriuresis was preceded by a corresponding increase in urinary PGE excretion (80%, 110% and 296%, respectively). The ... We propose that IL-1-induced natriuresis may be a component of the overall acute phase response which is actively mounted by ...
Characteristics of Norepinephrine Induced Natriuresis in Rabbits | Korean Journal of Nephrology;: 872-881, 2001. | WPRIM
April 1996 - Volume 14 - Issue 4 : Journal of Hypertension
Frontiers | How Do Antihypertensive Drugs Work? Insights from Studies of the Renal Regulation of Arterial Blood Pressure |...
What the Pressure-Natriuresis Line Tells us about Renal Hemodynamics. Kimura and colleagues examined the pressure-natriuresis ... Ivy, J. R., and Bailey, M. A. (2014). Pressure natriuresis and the renal control of arterial blood pressure. J. Physiol. 592(Pt ... A renal pressure-natriuresis line (sometimes called a "renal function curve") was plotted using these two data points and ... Kaloyanides, G. J., DiBona, G. F., and Raskin, P. (1971). Pressure natriuresis in the isolated kidney. Am. J. Physiol. 220, ...
IJMS | Free Full-Text | Diuretic Effects of Sodium Glucose Cotransporter 2 Inhibitors and Their Influence on the Renin...
However, in the early stages of treatment, these inhibitors frequently cause polyuria and natriuresis, which potentially ... However, in the early stages of treatment, these inhibitors frequently cause polyuria and natriuresis, which potentially ... Keywords: renin-angiotensin system (RAS); sodium glucose cotransporter 2 (SGLT2) inhibitor; diuretic effect; natriuresis; type ... 2 diabetes renin-angiotensin system (RAS); sodium glucose cotransporter 2 (SGLT2) inhibitor; diuretic effect; natriuresis; type ...