1988Clinical and Experimental HypertensionRequires access

Atrial Natriuretic Peptide in Volume Expansion-Induced Natriuresis in Man

Tivadar Tulassay, Heikki Ruskoaho, Miklós Tóth, Wolfgang Rascher

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Abstract

The role of atrial natriuretic peptide (ANP) in the extracellular volume expansion (ECVE) induced natriuresis was examined in normal man under basal conditions and following dopamine blockage. Hypotonic ECVE was induced by drinking of 20 ml/kg tap water and subsequent intravenous infusion of 2 1 0, 9% saline over a period of 4 hours. This maneuver caused an increase in the plasma concentrations of ANP from 25.8 +/- 3.4 (means +/- SEM) to 59.7 +/- 6.7 fmol/ml. There was a dissociation between ANP response and urinary sodium excretion. A transient rise in glomerular filtration rate (GFR), plasma dopamine and a continuous decrease in plasma renin activity, aldosterone, vasopressin, and noradrenaline were observed. The natriuretic response to ECVE was blunted during dopamine blockade by metoclopramide, but plasma ANP, renin activity, catecholamine and vasopressin levels were not affected. However, plasma aldosterone rose. Our data are compatible with the concept that intrarenal dopamine and raised plasma concentration of ANP contribute to the natriuretic response to ECVE, but these hormonal changes do not completely explain the underlying mechanisms.

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What this paper is about

The role of atrial natriuretic peptide (ANP) in the extracellular volume expansion (ECVE) induced natriuresis was examined in normal man under basal conditions and following dopamine blockage. Hypotonic ECVE was induced by drinking of 20 ml/kg tap water and subsequent intravenous infusion of 2 1 0, 9% saline over a period of 4 hours. This maneuver caused an increase in the plasma concentrations of ANP from 25.8 +/- 3.4 (means +/- SEM) to 59.7 +/- 6.7 fmol/ml. There was a dissociation between ANP response and urinary sodium excretion. A transient rise in glomerular filtration rate (GFR), plasma dopamine and a continuous decrease in plasma renin activity, aldosterone, vasopressin, and noradrenaline were observed. The natriuretic response to ECVE was blunted during dopamine blockade by metoclopramide, but plasma ANP, renin activity, catecholamine and vasopressin levels were not affected. However, plasma aldosterone rose. Our data are compatible with the concept that intrarenal dopamine and raised plasma concentration of ANP contribute to the natriuretic response to ECVE, but these hormonal changes do not completely explain the underlying mechanisms.

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Available abstract

The role of atrial natriuretic peptide (ANP) in the extracellular volume expansion (ECVE) induced natriuresis was examined in normal man under basal conditions and following dopamine blockage. Hypotonic ECVE was induced by drinking of 20 ml/kg tap water and subsequent intravenous infusion of 2 1 0, 9% saline over a period of 4 hours. This maneuver caused an increase in the plasma concentrations of ANP from 25.8 +/- 3.4 (means +/- SEM) to 59.7 +/- 6.7 fmol/ml. There was a dissociation between ANP response and urinary sodium excretion. A transient rise in glomerular filtration rate (GFR), plasma dopamine and a continuous decrease in plasma renin activity, aldosterone, vasopressin, and noradrenaline were observed. The natriuretic response to ECVE was blunted during dopamine blockade by metoclopramide, but plasma ANP, renin activity, catecholamine and vasopressin levels were not affected. However, plasma aldosterone rose. Our data are compatible with the concept that intrarenal dopamine and raised plasma concentration of ANP contribute to the natriuretic response to ECVE, but these hormonal changes do not completely explain the underlying mechanisms.

Key concepts: Natriuresis, Internal medicine, Atrial natriuretic peptide, Endocrinology, Plasma renin activity, Vasopressin, Aldosterone, Chemistry

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