Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “NATRIURESIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed1996

Role of volume status in vasopressin-induced natriuresis: studies in Brattleboro rats.

The influence of volume status on the effect of physiological doses of vasopressin on sodium excretion was assessed in anaesthetized Brattleboro rats. Following a 1 h control period, animals were divided into four groups. Group 1 (control) rats were kept in water balance throughout (by adjustment of the rate of i.v. glucose infusion) and received no vasopressin. In group 2 rats, vasopressin (20 microU/min) was infused i.v. for 2 h, then withdrawn during the following 2 h; the vasopressin-induced antidiuresis and subsequent return to water diuresis were matched by appropriate changes in the i.v. infusion, thus maintaining water balance. In this group, vasopressin had no effect on sodium excretion. Group 3 rats received the same dose of vasopressin, but the infusion rate of the glucose solution was not reduced; consequently these rats became water-loaded. In this group, sodium excretion increased significantly during vasopressin infusion, and rapidly returned to baseline values when the vasopressin was discontinued. Group 4 rats were treated in the same way as group 3 animals except that the vasopressin infusion was maintained (but without additional water loading) for a further 2 h; this did not prevent the fall in sodium excretion during the final 2 h of the experiment. We conclude that the natriuretic effect of physiological levels of vasopressin reported elsewhere may be dependent on an accompanying acute volume expansion during infusion of the hormone.

Animals↗
PubMed1990

Greater loop chloride uptake contributes to blunted pressure natriuresis in Dahl salt sensitive rats.

A blunted pressure natriuretic response is present in Dahl salt sensitive rats. To determine whether this results from tubular or glomerular mechanisms, late proximal, early distal, and late distal micropuncture were performed in salt resistant (R), salt sensitive (S), or salt sensitive rats with renal perfusion reduced to that of R rats (S-AC). Differences in neuro-endocrine background between groups were eliminated by renal denervation and by fixing plasma aldosterone, norepinephrine, and vasopressin levels by infusion. Renal perfusion pressure was greater (P less than 0.05) and inulin clearance less (P less than 0.05) in S than R rats. Urinary sodium excretion, however, was not different. S-AC had renal perfusion pressures that were similar to R rats and inulin clearance similar to S rats. Urinary NaCl excretion was less (P less than 0.05) than either group. Single nephron inulin clearance, fluid, and chloride delivery to late proximal sites were not different between groups. Absolute and fractional chloride delivery to early distal sites was less (P less than 0.05) in S-AC than R or S but not different between R and S. Late distal chloride delivery was not different between any group. Calculated loop chloride reabsorption was greater in S-AC than R or S. Thus, the lower urinary NaCl excretion in S-AC rats is in part due to increased loop chloride reabsorption. This effect is probably intrinsic to the S kidney as it occurs despite renal denervation when plasma levels of vasopressin, norepinephrine, and aldosterone are fixed. The increased loop chloride uptake is abolished when perfusion pressure increases.

Animals↗
PubMed1992

Potassium chloride lowers blood pressure and causes natriuresis in older patients with hypertension.

Epidemiologic surveys, experimental studies in animals, and clinical trials in young and middle-aged patients with hypertension indicate that dietary potassium lowers blood pressure. The mechanism of the antihypertensive effect is not well defined. Variations in serum potassium within the physiologic range may directly affect vascular smooth muscle tone. Potassium may also influence the regulation of blood pressure through effects on sodium handling, aldosterone secretion, the renin/angiotensin system, renal kallikrein, eicosanoids, and atrial natriuretic peptide. This study was undertaken to confirm the blood pressure-lowering effect of potassium in older patients and to determine the mechanism of the antihypertensive effect. Twenty-two patients greater than or equal to 60 yr of age were admitted to a Clinical Research Unit for 8 days after a 2-wk period free of antihypertensive medication. Patients were placed on an isocaloric diet containing 200 mmol/day of Na+, 70 mmol/day of K+, and 500 mg/day of Ca2+ and were treated in a randomized, double-blinded manner with either potassium chloride (120 mmol/day) or placebo. After 4 days, patients were crossed over to the alternate treatment. Systolic blood pressure decreased 8.6 mm Hg (95% confidence interval -14.6, -2.6), and diastolic blood pressure decreased 4.0 mm Hg (-6.9, -1.0) during potassium chloride supplementation. There was no significant change in blood pressure during treatment with placebo. Serum K+ was 3.9 +/- 0.1 mmol/L after 3 days of placebo and 4.3 +/- 0.1 after 4 days of potassium chloride (P less than 0.002). Urinary sodium excretion averaged 192 +/- 11 mmol/day after placebo and 221 +/- 8 after potassium treatment (P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1998

Novel angiotensin peptides regulate blood pressure, endothelial function, and natriuresis.

Accumulating evidence suggests that angiotensin-(1-7) is an important component of the renin-angiotensin system, having actions that are either identical to or opposite that of angiotensin II. Angiotensin I can be directly converted to angiotensin-(1-7), bypassing formation of angiotensin II. This pathway is under the control of three enzymes: neutral endopeptidases 24.11 (neprilysin) and 24.15 and prolyl-endopeptidase 24.26. Two of the three angiotensin-forming enzymes (neprilysin and endopeptidase 24.15) also contribute to the breakdown of bradykinin and the atrial natriuretic peptide. Furthermore, angiotensin-(1-7) is a major substrate for angiotensin-converting enzyme. These observations suggest that the process of biotransformation between the various Ang peptides of the renin-angiotensin system and other vasodepressor peptides are intertwined through this enzymatic pathway. Substantial evidence suggests that angiotensin-(1-7) stimulates the synthesis and release of vasodilator prostaglandins, and nitric oxide, while also augmenting the metabolic actions of bradykinin. In addition, angiotensin-(1-7) alters tubular sodium and bicarbonate reabsorption, decreases Na+-K+-ATPase activity, induces diuresis, and exerts a vasodilator effect. These physiologic effects of angiotensin-(1-7) favor a blood pressure-lowering effect. The majority of the data currently available suggest that angiotensin-(1-7) mediates its effects through a novel non-AT1/AT2 receptor subtype.

Angiotensin II↗
PubMed1977

Inhibition of furosemide-induced natriuresis by acetylsalicylic acid in dogs.

The effect of intravenously administered acetylsalicylic acid (ASA) has been investigated in two sets of experiments in conscious dogs. In the first part of the study ASA 70-90 mg/kg was infused for 40 min. Urine flow, free water clearance, renal blood flow and urinary excretion of sodium did not change significantly as compared to placebo treated animals. This is in contrast to the effects of comparable ASA doses in the pentobarbital anaesthetized dog. In the second part of the study the effects of pre-treatment with the same ASA doses of 5 ml 0.6% NaCl (placebo) on some renal effects of furosemide 1 mg/kg (intravenously) were investigated. In the placebo group acute furosemide treatment increased CIN in five out of six dogs and CPAH in all six dogs, these increases being most prominent the first 10 min after drug administration. After pre-treatment with ASA the initial increases in CIN and CPAH were almost abolished. CIN was reduced by 23.8% and CPAH by 30.6% during the first six clearance periods (0-6- min) after diuretic treatment in the ASA group as compared to the placebo group. Although urinary sodium excretion also increased in ASA pre-treated dogs, the effect of furosemide was greater in all dogs in the placebo group (P less than 0.05), and the effect of furosemide on fractional tubular reabsorption of sodium was significantly attenuated after pre-treatment with ASA.

Animals↗
PubMed1995

Vesical-renal reflex: diuresis and natriuresis activated by intravesical capsaicin.

In the last years the role of capsaicin sensitive innervation, in the activation of the micturition reflex, has been reported in many papers. In our experience, upon the intravesical administration of capsaicin in humans, we noticed an increase of diuresis. No interaction is known about the sensory innervation of the bladder and renal function, so we studied the possibility of the existence of a vesical-renal reflex arc. Twenty-one patients (9 men and 12 women) were randomised to receive intravesical infusion of saline solution containing 10 microM capsaicin. Urine output, glomerular renal filtrate (GRF) and effective plasma renal flow (EPRF), measured by Technetium-99m diethylenetetramine-penta-acetic acid (DTPA) renal scintigraphy, were recorded over twenty minutes before and after the intravesical administration of capsaicin. Urine density, [Na+] and [K+] concentration, and prostaglandin E2 excretion were also determined before and after intravesical administration of capsaicin or vehicle. Installation of saline solution containing 10 microM capsaicin produced a significant increase of mean urine output, an increase of GRF, of EPRF and of [Na+] and [K+] urine concentration. An increase, not statistically significant, was observed of PgE2 excretion. None of the patients treated with vehicle showed any modification of parameters examined. The present findings demonstrate a hitherto unrecognized effect: increased diuresis following selective chemical stimulation of bladder efferents with capsaicin. The renal diuretic response to intravesical capsaicin represents a working hypothesis about the possible involvement of a vesical-renal reflex arc organized at spinal or supraspinal level.

Administration, Intravesical↗
PubMed1997

Circadian variation in the natriuresis produced by potassium intake in the rat.

To determine if there was an endogenous circadian regulation of the renal natriuretic response to acute potassium loading, unanesthetized rats, either fed or fasted, were given an intragastric infusion of KCl over 100 min at the times of maximum and minimum circadian sodium excretion, i.e. in the early dark and early light phase of a 12 hour dark/light cycle. During KCl infusion plasma potassium concentration as well as sodium and potassium excretion progressively increased. Cumulative sodium excretion was greater in dark than light phase, and was greater in fed than fasted rats. Sodium excretion was greater at any given elevated level of plasma potassium in the dark than light phase. The results suggest that reported variations in the effects of high potassium diets on sodium excretion, blood pressure, or circulatory pathology in hypertension, may in part be explained by variations in the time of oral potassium intake.

Animals↗
PubMed1998

Renal nerves and D1-dopamine receptor-mediated natriuresis.

The resistance of the spontaneously hypertensive rat (SHR) kidney to the natriuretic effect of dopamine and D1 agonists may be due to increased renal nerve activity. Therefore, we compared the effects of the intrarenal arterial infusion of the D1 agonist, SKF 38383, into the denervated (DNX) kidney of saline-loaded-anesthetized SHR and its control, the Wistar-Kyoto (WKY) rat. In both WKY and SHR, DNX of the left kidney slightly decreased urine flow (UV) and absolute (UNaV) and fractional sodium excretion (FENa) in the innervated right kidney; neither vehicle nor D1 agonist infusion exerted any effect. In the left kidney, denervation increased UV, UNaV, and FENa to a similar degree in WKY and SHR (2-fold), without affecting renal blood flow, glomerular filtration rate, or blood pressure. In WKY but not in SHR, after DNX, the D1 agonist dose-dependently increased UV, UNaV, and FENa in the denervated kidney. We conclude that the decreased natriuretic effect of D1 agonists in the SHR is not due to increased renal nerve activity. These data support our previous studies implicating a defect of the D1 receptor or its regulation in the kidney in genetic hypertension.

Animals↗
PubMed1979

Reinvestigation of denervation diuresis and natriuresis in conscious dogs.

The function of innervated and denervated kidney was compared in clearance studies with conscious dogs. The animals were prepared for experiments by unilateral renal denervation and surgical division of the bladder to form two hemibladders enabling separate urine collection from two kidneys. The mean urine flow was 6% higher for the denervated kidney (not significant) while mean differences for osmolar clearance (+ 13%), sodium excretion (+21%) and GFT (+5%) were all significant (P less than 0.05). When corrected to 100 ml GFR, sodium excretion was not significantly higher for the denervated kidney. In most experiments higher sodium excretion on the denefvated side was associated with higher GFR. Thus, contrary to some earlier views, a slight increase in the excretory function which follows denervation of the kidney is demonstrable also in conscious undisturbed animals. The data suggest that increased haemodynamics of the denervated kidney are responsible for higher excretion, but do not exclude a contribution of inhibited tubular reabsorption.

Animals↗