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Aldosterone Response to Long Term Infusion of Angiotensin II and Angiotensin III in Conscious Dogs before and after Dietary Sodium Restriction^*

Department of Physiology and Biophysics, University of Mississippi School of Medicine Jackson, Mississippi

Address all correspondence and requests for reprints to: Robert E. McCaa, Ph.D., Professor of Physiology and Biophysics, Department of Physiology and Biophysics, University of Mississippi School of Medicine, 2500 North State Street, Jackson, Mississippi 39216.

Abstract

The aldosterone and arterial blood pressure response to long term infusion of angiotensin II (AII) and (des-asp¹)-angiotensin II (A-III) was studied in conscious dogs before and after dietary sodium restriction. Plasma aldosterone concentration (PAC), plasma cortisol concentration (PCC), and plasma renin activity (PRA) were determined by RIA. During long term infusion of A-II (15 ng/kg min^-1) in sodium-replete animals, PAC increased from 7.1 ± 2.9 ng/100 ml to a steady state level of 14.7 ± 4.6 ng/100 ml (mean ± SE; P < 0.01), PRA was undetectable by RIA, and arterial pressure increased from 103 ± 5 to 142 ± 8 mm Hg (P < 0.001). During long term infusion of A-III (30 ng/kg min^-1) in sodium-replete animals, PAC increased from 8.3 ± 3.4 ng/100 ml to a steady state level of 15.9 ± 5.2 ng/100 ml (P < 0.01), PRA decreased from 0.79 ± 0.21 to 0.61 ± 0.32 ng/ml/h (NS, P > 0.05), and arterial pressure failed to change from control levels of 103 ± 5 mm Hg. During long term infusion of A-II (15 ng/kg min^-1) in sodium-deplete animals, PAC increased from 36.3 ± 10.4 ng/100 ml to a steady state level of 94.3 ± 17.8 ng/100 ml (P < 0.01), while PRA and arterial pressure remained near control levels. During long term infusion of A-III (30 ng/kg min^-1) in sodium-deplete animals, PAC increased from 39.1 ± 9.8 ng/100 ml to a steady state level of 79.9 ± 16.7 ng/100 ml (P < 0.01), while PRA and arterial pressure remained near control levels. These data demonstrate that the adrenal glomerulosa response to angiotensin II and (des-asp¹)-angiotensin II is markedly increased during sodium deficiency and support the concept that increased aldosterone biosynthesis during sodium deficiency is mediated in part by increased activity of the renin-angiotensin system.

Footnotes

^* This investigation was supported by USPHS Grants HL-09921 and HL-11678 from the NIH and by a grant from the Mississippi Heart Association.

Received July 21, 1977.

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