Studies on the mechanism of natriuresis accompanying increased renal blood flow and its role in the renal response to extracellular volume expansion.

Earley, Laurence E.; Friedler, Robert M.

doi:10.1172/jci105293

Cited by 106 publications

(63 citation statements)

References 13 publications

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“…These results are in agreement with the work of Johnson and Freeman (2 1), who previously suggested that systemic inhibition of NO synthase produces a pressure-dependent natriuresis. The results of study I are also consistent with previous reports of a natriuretic effect of agonists ofthe EDRF, NO, such as acetylcholine (33,34); as well as the work of Alberola et al (39) in which it was reported that, in the dog, the natriuresis and diuresis induced by extracellular volume expansion with saline was blunted during intrarenal L-NAME infusion. These previous studies suggest that stimulation of NO activity increases renal sodium excretion.…”

Section: Discussionsupporting

confidence: 90%

“…In experimental animals acetylcholine infusion results in decreased systemic blood pressure, a large increase in glomerular capillary plasma flow, but no change in single-nephron GFR, resulting in a fall in filtration fraction (32,33). Acetylcholine infusion has also been reported to have a diuretic and natriuretic effect (33,34). Lahera et al (35) reported that this acetylcholine-induced diuretic effect was dependent on intact NO synthase activity.…”

Section: Discussionmentioning

confidence: 99%

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Adaptation to increased dietary salt intake in the rat. Role of endogenous nitric oxide.

Shultz¹,

Tolins²

1993

J. Clin. Invest.

241

149

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Previous studies have suggested that nitric oxide (NO) plays a role in regulation of renal vascular tone and sodium handling.We questioned whether the effects of NO synthase inhibition on renal function are direct or due to increased renal perfusion pressure (RPP) and whether stimulation of endogenous NO activity plays a role in adaptation to increased dietary salt intake. Intrarenal arterial infusion of the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) in control rats resulted in decreased glomerular filtration rate, renal vasoconstriction, natriuresis, and proteinuria. When RPP was held at basal levels with a suprarenal aortic snare, L-NMMA had similar hemodynamic effects but decreased sodium excretion and did not induce proteinuria. Exposure of rats to high salt intake (1% NaCl drinking water) for 2 wk induced increased serum concentration and urinary excretion of the NO decomposition products, NO2 + NO3. Urinary NO2 + NO3 and sodium excretion were significantly correlated. Compared with controls, chronically salt-loaded rats also demonstrated enhanced renal hemodynamic responses to NO synthase inhibition. We conclude that the endogenous NO system directly modulates renal hemodynamics and sodium handling and participates in the renal adaptation to increased dietary salt intake. Enhanced NO synthesis in response to increased salt intake may facilitate sodium excretion and allow maintenance of normal blood pressure. (J. Clin. Invest. 1993. 91:642-650.)

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Adaptation to increased dietary salt intake in the rat. Role of endogenous nitric oxide.

Shultz¹,

Tolins²

1993

J. Clin. Invest.

241

149

View full text Add to dashboard Cite

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“…We recently suggested that increased renal blood flow, and perhaps increased medullary blood flow specifically, may be one factor that by way of intrarenal mechanisms contributes to diminished reabsorption of sodium during saline loading (5). Furthermore, natriuresis in the absence of salt loading accompanies increased renal blood flow when local vasodilatation is produced by a variety of agents (7)(8)(9)(10)(11)(12)(13), and we have observed that the unilateral natriuresis accompanying increased renal blood flow during the renal arterial infusion of acetylcholine is due in part to diminished net tubular reab-sorption of sodium (14). Leyssac has suggested that angiotensin may depress proximal tubular reabsorption (15), and it has been demonstrated that under certain conditions angiotensin may produce natriuresis (16)(17)(18)(19).…”

mentioning

confidence: 83%

The effects of combined renal vasodilatation and pressor agents on renal hemodynamics and the tubular reabsorption of sodium.

Earley¹,

Friedler²

1966

J. Clin. Invest.

Self Cite

214

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“…Net renin secretion was calculated by the following formula: (renal venous plasma renin activity -arterial plasma renin activity) renal plasma blood flow. Inulin was determined colorimetrically by reaction with anthrone in H2SO4 (Davidson & Sackner 1963) by a technique adapted for the Technicon Autoanalyzer (Earley & Friedler, 1965). Urine sodium and potassium concentration was determined by flame photometry.…”

Section: Experimental Designmentioning

confidence: 99%

The role of histamine receptors in the release of renin

Gerber

Nies

1983

British J Pharmacology

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1 The effect of intrarenal histamine, dimaprit (H2-agonist) and 2-(2-pyridyl) ethylamine (Hl-agonist) on renin release was examined in anaesthetized dogs.2 In dogs with intact kidneys, histamine and dimaprit administration resulted in renal vasodilatation, a two fold increase in urinary sodium excretion, and no change in renal renin release. 2(2-Pyridyl) ethylamine administration resulted in renal vasodilatation, a 25% decrease in urinary sodium excretion and a significant increase in renin release. 3 In dogs with non-filtering kidneys, dimaprit administration resulted in renal vasodilatation and a significant increase in renin release, while 2(2-pyridyl) ethylamine administration resulted in renal vasodilatation but no change in renin release. 4 Our data suggest that histamine is a potential participant in the release of renin through stimulation of H2-receptors, but it is a weak agonist. 5In addition, the direct effect of histamine analogues on renin release is modulated by their effects on electrolyte excretion probably by influencing the renal chemoreceptor release of renin mediated by the macula densa.

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Studies on the mechanism of natriuresis accompanying increased renal blood flow and its role in the renal response to extracellular volume expansion.

Cited by 106 publications

References 13 publications

Adaptation to increased dietary salt intake in the rat. Role of endogenous nitric oxide.

Adaptation to increased dietary salt intake in the rat. Role of endogenous nitric oxide.

The effects of combined renal vasodilatation and pressor agents on renal hemodynamics and the tubular reabsorption of sodium.

The role of histamine receptors in the release of renin

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