Effect of angiotensin on renal function in the rat

Barraclough, M. A.; Nf, Jones; Marsden, C. D.

doi:10.1152/ajplegacy.1967.212.5.1153

Cited by 78 publications

(72 citation statements)

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“…It could be thought that this fall of MBP and increase of PRA depend upon natriuresis caused by aldosterone antagonist as well as by increased kallikrein activity. Kinins are known as one of the most potent vasodilators; when infused in the renal artery kinins produce marked natriuresis (Webster and Gilmore 1964; Barraclough and Mills 1965;Stein et al 1972). It may be thought that increased kallikrein after the spironolactone treatment in low renin essential hypertension produces kinin in the renal cortex, and these kinins are released to peritubular interstitial space or peritubular capillary circulation.…”

Section: Discussionmentioning

confidence: 99%

Effect of spironolactone on urinary kallikrein excretion in patients with essential hypertension and in primary aldosteronism.

Seino

Abe

Sakurai

et al. 1977

Tohoku J. Exp. Med.

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Section: Discussionmentioning

confidence: 99%

Effect of spironolactone on urinary kallikrein excretion in patients with essential hypertension and in primary aldosteronism.

Seino

Abe

Sakurai

et al. 1977

Tohoku J. Exp. Med.

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“…Many studies in intact animals have indicated that kinins are natriuretic (2)(3)(4)(5). However, it is unclear whether natriuresis results from the hemodynamic effects of kinins or from a direct renal tubular action on sodium transport.…”

Section: Introductionmentioning

confidence: 99%

Control of sodium and potassium transport in the cortical collecting duct of the rat. Effects of bradykinin, vasopressin, and deoxycorticosterone.

Tomita¹,

Pisano²,

Knepper³

1985

J. Clin. Invest.

279

164

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Several factors interact to maintain precise control of electrolyte transport in the mammalian cortical collecting duct. We have studied the effects of deoxycorticosterone, arginine vasopressin, and bradykinin on net transepithelial sodium and potassium transport in isolated, perfused rat cortical collecting ducts. Chronic administration of deoxycorticosterone to rats increased both sodium absorption and potassium secretion above very low basal levels. Consequently, deoxycorticosterone-treated rats were used for all remaining studies. Arginine vasopressin (10-10 M in the bath) caused a sustained fourfold increase in net sodium absorption and a sustained threefold increase in net potassium secretion. Bradykinin (10-9 M in the bath) caused a reversible 40-50% inhibition of net sodium absorption without affecting net potassium transport or the transepithelial potential difference. In the perfusate, up to 10-6 M bradykinin had no effect. We conclude: (a) As in rabbits, chronic deoxycorticosterone administration to rats increases sodium absorption and potassium secretion in cortical collecting ducts perfused in vitro. (b) Arginine vasopressin causes a reversible increase in net potassium secretion and net sodium absorption. (c) Bradykinin in the peritubular bathing solution reversibly inhibits net sodium absorption, possibly by affecting an electroneutral sodium transport pathway.

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“…Recently, it has been reported that prolactin has water -sodium retaining action (Horrobin et al 1971;Buckman et al . 1976) and that the renal kallikrein kinin system has a water diuretic and naturiuretic action (Barraclough and Mills 1965;Marin-Grez et al . 1972;Mills et al 1976).…”

Section: Resultsmentioning

confidence: 99%