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At least 577 records · Page 32Linked to original sources
PubMed1992

Natriuresis after a water load in humans under different sodium body content.

The present study was aimed at observing the diuretic and natriuretic responses after a water load (2% body weight) in four groups of young consenting volunteers submitted previously, during three days, to a hypersodic (500 mEq Na/day), hyposodic (35 mEq Na/day), and normosodic (200 mEq Na/day) diet, or treated with furosemide (Lasix, 40 mg/day). During the treatment urine was collected each day. On the fourth day, in the morning, the bladder was emptied, the water load was ingested, and the urine collected during 10 periods of 20 min each. The urinary, sodium, and chloride flows were determined. The four groups displayed diuretic curves following a similar pattern. In contrast, the natriuretic curves of the four groups were completely different; totally flat with low values for the furosemide group and a large initial natriuretic curve for the hypersodic group with a gradual decrease but maintaining high values. The results indicate that the way the organism compensates for the excess of water by means of urinary water loss is independent of the body sodium content, whereas the way in which sodium loss is accomplished is determined by its body content and is independent of the way in which the water is lost.

Adult↗
PubMed1987

Effect of diabetes on natriuresis in the presence of ouabain and ethacrynic acid in perfused rat kidney.

1. The effect of diabetes on renal sodium retention was investigated. 2. The technique involved retrograde perfusion from the renal veins via the kidneys, and then through the renal arteries and dorsal aorta. 3. Sodium retention by diabetic rat kidney was 58% lower than that in the normal rats. 4. Ouabain (15 mM) in perfusate increased sodium retention by 30% in normal rat kidney as compared to a 54% increase in diabetic rat kidney. 5. Ethacrynic acid (1 mM) in perfusate resulted in a 42% reduction in sodium retention in the normal rat kidney as compared to a 43% decrease in the diabetic rat kidney. 6. Control of hyperglycemia in diabetic rats with insulin therapy resulted in sodium retention that is not significantly different from that of normal rats. 7. The results suggest that diabetes has no effect on the peritubular ouabain-sensitive Na--K-ATPase pump, or the luminal ethacrynic acid-sensitive Na-K counter transport pump. Furthermore, the data suggest a reversible effect of diabetes on sodium retention during insulin therapy.

Animals↗
PubMed1986

Centrally mediated effect of vanadate on diuresis and natriuresis in normal rats. Interaction with ouabain.

Prolonged infusion of vanadate (VO-3) (51 ng/microliter/hr during 15 hr), an in vitro inhibitor of Na,K-ATPase activity, into the 3rd brain ventricle (3BV) increased diuresis, sodium and potassium excretion in normal rats (p less than 0.001). Since the animals did not receive food or water during the infusion period, the effect of VO-3 was not related to hydration or volume expansion. A single injection of ouabain (a specific inhibitor of the sodium pump) 1 microliter, 50 pg/microliter, followed by a single injection of vanadate (1 microliter/51 ng/microliter) 1, 5 or 10 minutes after ouabain, prevented the diuretic and natriuretic effect of VO-3. When vanadate injections were delayed 20 or 30 minutes, diuresis reappeared. Ouabain (50 pg) decreased sodium intake induced by sodium depletion, an effect that lasted for 10 to 15 minutes after injection, a time coincident with the inhibition of the natriuretic effect of VO-3 by OUA. Then the life-span of ouabain effect on prevention of VO-3-induced diuresis as well as on inhibition of sodium intake, lasted between 10 to 15 minutes. These results provide further evidence for the powerful diuretic, natriuretic and kaliuretic effect of centrally injected vanadate. However, the finding that ouabain suppresses this effect, does not support the suggestion that the active transport system might be involved.

Animals↗
PubMed2005

Amylin induces natriuresis by a central angiotensin-dependent mechanism.

This study provides evidence that amylin acts centrally to increase sodium excretion in the sheep. Amylin was infused at 8 mg/h into a carotid artery (IC), via a lateral ventricle (ICV), intravenously (IV) or intra-renally (IR) into conscious sheep (n=5 per group). Renal sodium excretion increased by at least 3-fold after 1 h of amylin infusion by ICV (66+/-14 to 367+/-35 mmol/min) and IC (78+/-14 to 244+/-22 mmol/min) routes of administration. Amylin infusion IV caused a 1.5-fold increase in sodium excretion while IR infusion did not have a significant effect. The natriuretic effect of ICV infused amylin was blocked by pre-treatment with the angiotensin AT1 receptor antagonist, losartan (1 mg/h). No changes in blood pressure or heart rate were recorded at this dose of amylin by any route of administration. Plasma renin concentration increased (1.32+/-0.22 to 2.55+/-0.73 pmol/Ang I/h; P<0.05) following IR infusion of amylin, and remained unchanged when amylin was infused by the other routes of administration. We conclude that amylin causes changes in sodium excretion in sheep through a central, angiotensin-dependent pathway and that amylin may increase renin secretion by a direct effect on the kidney.

Amyloid↗
PubMed1998

Diuresis and natriuresis produced by long term administration of a selective Angiotensin-(1-7) antagonist in normotensive and hypertensive rats.

In this study we evaluated the renal effects of chronic administration of the selective Angiotensin-(1-7)[Ang-(1-7)] antagonist, A-779, in normotensive and spontaneously hypertensive rats (SHR). Male adult SHR and Wistar rats were housed in metabolic cages with tap water and standard chow, for three-five days before starting infusion (Alzet osmotic mini-pumps) of A-779 (Wistar: 1 microg/h, n = 9; 2.5 microg/h, n = 6; SHR:2.5 microg/h, n = 6) or vehicle (0.9% NaCl - 1 microl/h, n = 7 and n = 10 for SHR and Wistar rats, respectively). Urine volume, water and food intake and urinary Na+ were measured daily. On the last day of infusions mean arterial pressure (MAP) was recorded and urine and blood samples were collected to determine renal function parameters. Chronic infusion of A-779 produced a sustained increase in diuresis in normotensive rats [seventh day values: 0.75+/-0.08 ml/h (1 microg/h) and 0.94+/-0.13 ml/h (2.5 microg/h) vs. 0.42 + 0.03 ml/h for the control group, P<0.05] associated to a dose-dependent increase in the creatinine clearance. In SHR, diuresis increased significantly after chronic infusion of A-779 (fifth day values: 0.44 + 0.06 ml/h vs. 0.25+/-0.04 ml/h for the control group, P<0.05), without changes in creatinine clearance. Infusion of A-779 in normotensive rats produced a decrease in water reabsorption. A-779 infusion also produced a dose-dependent increase in urinary Na+ excretion (1.49 + 0.14 mEq, 1 microg/h vs. 2.37+/-0.22 mEq, 2.5 microg/h, P<0.05), in Wistar rats, without modifying the fractional excretion of Na+. In SHR, urinary Na+ excretion was also increased by A-779 (2.21+/-0.46 mEq vs. 0.94+/-0.22 mEq for the control group, P<0.05). No significant changes in blood pressure were observed. These findings suggest that endogenous Ang-(l-7) participates in the control of hydroelectrolyte balance by modulating water excretion, acting at tubular and glomerular sites.

Angiotensin I↗
PubMed2001

A role for the angiotensin IV/AT4 system in mediating natriuresis in the rat.

Angiotensin II (AngII) or Angiotensin IV (AngIV) was infused into the renal artery of anesthetized rats while renal cortical blood flow was measured via laser Doppler flowmetry. The infusion of AngII produced a significant elevation in mean arterial pressure (MAP) with an accompanying decrease in cortical blood flow, glomerular filtration rate (GFR), urine volume, and urine sodium excretion. The infusion of AngIV induced significant increases in renal cortical blood flow and urine sodium excretion, without altering MAP, GFR, and urine volume. Pretreatment infusion with a specific AT1 receptor antagonist, DuP 753, blocked or attenuated the subsequent AngII effects, while pretreatment infusion with the specific AT4 receptor antagonist, Divalinal-AngIV, blocked the AngIV effects. These results support distinct and opposite roles for AngII and AngIV, i.e. AngII acts as an anti-natriuretic agent, while AngIV acts as a natriuretic agent.

Angiotensin II↗
PubMed2003

Role of brain dopaminergic system in the adrenomedullin-induced diuresis and natriuresis.

Intracerebroventricular (IVT) administration of adrenomedullin (AM) to conscious male hydrated rats increases urinary volume and sodium excretion. The possible involvement of brain dopamine (DA) system on the renal action of IVT-AM was investigated. AM-induced diuretic and natriuretic action was prevented following selective central dopaminergic denervation with 6-hydroxydopamine (6OHDA) in combination with desmethylimipramine (DMI). Selective D(2) DA receptor antagonism with haloperidol, sulpiride, and remoxipride; or with the D(1) DA receptor antagonist, SCH 23390, blunted the increase in urinary volume and sodium excretion induced by IVT-AM. The present results suggest that AM acts centrally, at least in part, via an interaction with endogenous DA through the activation of both DA D(1)/D(2) receptor subtype.

Adrenergic Uptake Inhibitors↗