Renal blockade to angiotensin II in acute and chronic sodium retaining states

Gary Slick, G. F. DiBona, G. J. Kaloyanides

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Acute thoracic inferior vena cava constriction results in alterations in renal hemodynamics which may explain the characteristic antinatriuretic response. Since adrenal vein aldosterone secretion is increased within 30 min of acute caval constriction and elevated plasma renin activity is found in the chronic caval dog, we sought to determine whether the renal hemodynamic alterations observed in acute caval constriction are due to the intrarenal action of angiotensin II. The renal response to acute caval constriction in dogs receiving unilateral renal arterial infusion of a specific competitive antagonist of angiotensin II. II, sarcosine 8 alanine angiotensin II, was studied. Effective blockade did not alter the renal hemodynamic or antinatriuretic response to acute caval constriction. As a model of chronic sodium retention, dogs with chronic congestive heart failure produced by tricuspid insufficiency and pulmonary stenosis were similarly studied. Effective renal blockade to angiotensin II did not affect renal hemodynamics or urinary sodium excretion. The renal hemodynamic and antinatriuretic responses to acute caval constriction and chronic congestive heart failure are not dependent on the intrarenal action of angiotensin II.

Original languageEnglish
Pages (from-to)185-193
Number of pages9
JournalJournal of Pharmacology and Experimental Therapeutics
Volume195
Issue number2
StatePublished - 1 Dec 1975

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Angiotensin II
Venae Cavae
Sodium
Constriction
Kidney
Hemodynamics
Dogs
Heart Failure
Sarcosine
Pulmonary Valve Stenosis
Inferior Vena Cava
Aldosterone
Renin
Veins
Thorax

Cite this

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Renal blockade to angiotensin II in acute and chronic sodium retaining states. / Slick, Gary; DiBona, G. F.; Kaloyanides, G. J.

In: Journal of Pharmacology and Experimental Therapeutics, Vol. 195, No. 2, 01.12.1975, p. 185-193.

Research output: Contribution to journalArticle

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