Renal autoregulation, filtration rate, and electrolyte excretion during vasodilatation

Baer, P G; Navar, L. G.; Guyton, Arthur C.

doi:10.1152/ajplegacy.1970.219.3.619

Cited by 62 publications

(35 citation statements)

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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: 91%

“…Tolins and coworkers ( 14) recently demonstrated that the renal hemodynamic effects ofacetylcholine in vivo are also mediated by the EDRF, NO. 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).…”

Section: Discussionmentioning

confidence: 99%

“…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.

242

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: 91%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

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

Shultz¹,

Tolins²

1993

J. Clin. Invest.

242

149

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“…The decrease in GFR caused by papaverine has been reported by Baer et al (13). These facts suggest that there are differences in vasodilating response between CRD-401 and papaverine.…”

Section: Discussionsupporting

confidence: 56%

Studies on a New 1, 5-Benzothiazepine Derivative (CRD-401)

Yamaguchi

Ikezawa

TAKADA

et al. 1974

Japanese Journal of Pharmacology

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-Effects of a new coronary vasodilator, CRD-401, on renal blood flow and renal function were investigated in anesthetized dogs. Renal arterial or systemic administration of the compound produced an increase in renal blood flow. The increase in renal blood flow induced by CRD-401 was not affected by pre-treatment with propranolol, atropine or dephenhydramine.Renal arterial administration of CRD-401 exhibited an antagonistic effect on the vasoconstricting action of angioten sin-II, whereas it had no effect on that of epinephrine.When infused continuously into the renal artery, CRD-40l increased the urine flow and sodium excretion as well as renal blood flow in all the conditions of fluid loading tested. The glomerular filtration rate was enhanced under saline loading but not under water diuresis. CRD 401 caused an increase in free water clearance. When the renal blood flow was kept constant with an aortic clamp during CRD-401 infusion, sodium excretion was signifi cantly increased but no change was observed in glomerular filtration rate and PAH clearance. The results show that CRD-401 induced natriuresis was not entirely dependent upon the renal hemodynamic changes caused by the compound.By the stop-flow method, it was shown that the ratio of [urine sodium to plasma sodium] to [urine creatinine to plasma creatinine] increased in the distal portion of the nephrun by CRD-401 infusion. The present results indicate that the natriuretic action of' CRD-401 is not only due to the changes in renal hemodynamics but it also may be ascribable to a direct effect of CRD-410 on the sodium reabsorption in the distal part of the nephron.

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“…NO has been shown to increase renal blood flow, enhance glomerular filtra- tion, regulate renin release, and inhibit salt transport along the nephron (6). In vivo studies have shown that stimulation of NO generation increases (2,22,23), whereas inhibition of NO production decreases, urinary volume and Na ϩ excretion (18 -20). Moreover, impaired NO system activity has been implicated in several forms of salt-sensitive hypertension (3,13,16).…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide inhibits basolateral 10-pS Cl⁻channels through the cGMP/PKG signaling pathway in the thick ascending limb of C57BL/6 mice

Gao

et al. 2016

American Journal of Physiology-Renal Physiology

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Wu P, Gao Z, Ye S, Qi Z. Nitric oxide inhibits basolateral 10-pS Cl Ϫ channels through the cGMP/PKG signaling pathway in the thick ascending limb of C57BL/6 mice. Am J Physiol Renal Physiol 310: F755-F762, 2016. First published January 13, 2016 doi:10.1152/ajprenal.00270.2015.-We used patch-clamp techniques to examine whether nitric oxide (NO) decreases NaCl reabsorption by suppressing basolateral 10-pS Cl Ϫ channels in the thick ascending limb (TAL). Both the NO synthase substrate L-arginine (L-Arg) and the NO donor S-nitroso-N-acetylpenicillamine significantly inhibited 10-pS Cl Ϫ channel activity in the TAL. The inhibitory effect of L-Arg on Cl Ϫ channels was completely abolished in the presence of the NO synthase inhibitor or NO scavenger. Moreover, inhibition of soluble guanylyl cyclase abrogated the effect of L-Arg on Cl Ϫ channels, whereas the cGMP analog 8-bromo-cGMP (8-BrcGMP) mimicked the effect of L-Arg and significantly decreased 10-pS Cl Ϫ channel activity, indicating that NO inhibits basolateral Cl Ϫ channels by increasing cGMP production. Furthermore, treatment of the TAL with a PKG inhibitor blocked the effect of L-Arg and 8-BrcGMP on Cl Ϫ channels, respectively. In contrast, a phosphodiesterase 2 inhibitor had no significant effect on L-Arg or 8-BrcGMP-induced inhibition of Cl Ϫ channels. Therefore, we conclude that NO decreases basolateral 10-pS Cl Ϫ channel activity through a cGMP-dependent PKG pathway, which may contribute to the natriuretic and diuretic effects of NO in vivo.thick ascending limb; nitric oxide; Cl Ϫ channel; cGMP; protein kinase G THE THICK ASCENDING LIMB (TAL) is responsible for the reabsorption of 25% of the filtered salt load and plays a key role in the urinary concentrating mechanism (7, 12). Excessive NaCl reabsorption by the TAL contributes to the development of hypertension (1). Approximately 20 -30% of reabsorbed Na ϩ and Cl Ϫ enter epithelial cells in the TAL through apical type II Na ϩ -K ϩ

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Renal autoregulation, filtration rate, and electrolyte excretion during vasodilatation

Cited by 62 publications

References 0 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.

Studies on a New 1, 5-Benzothiazepine Derivative (CRD-401)

Nitric oxide inhibits basolateral 10-pS Cl⁻channels through the cGMP/PKG signaling pathway in the thick ascending limb of C57BL/6 mice

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Renal autoregulation, filtration rate, and electrolyte excretion during vasodilatation

Cited by 62 publications

References 0 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.

Studies on a New 1, 5-Benzothiazepine Derivative (CRD-401)

Nitric oxide inhibits basolateral 10-pS Cl−channels through the cGMP/PKG signaling pathway in the thick ascending limb of C57BL/6 mice

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Nitric oxide inhibits basolateral 10-pS Cl⁻channels through the cGMP/PKG signaling pathway in the thick ascending limb of C57BL/6 mice