Atrial antipressor natriuretic peptide: release mechanisms and vascular action in man

Abstract

Atrial natriuretic peptide (ANP) release into the human circulation, responses to cardiopulmonary volume changes and natriuretic and vasorelaxant effects were studied in 45 normal subjects and in 12 patients during diagnostic cardiac catheterization. A new radioreceptor assay with a detection limit of 2 fmol/tube for alpha-human ANP (alpha-hANP) was used. In normal subjects plasma ANP was 27.2 +/- 4 pmol/l (n = 45, range 2-80). Right atrial plasma ANP correlated with right atrial pressure (r = 0.813, P less than 0.01), and in four of the patients increases in ANP paralleled the rise in atrial pressure during bicycle ergometry. Reducing venous return by bilateral thigh-cuff occlusion decreased atrial ANP from 66.8 +/- 17.9 to 19.6 +/- 8.0 pmol/l (n = 6, P less than 0.05). Increasing cardiopulmonary volume during 3-h head-out water immersion was associated with an increase in ANP from 16.0 +/- 5.6 to 92.6 +/- 21.5 pmol/l (n = 7, P less than 0.01) followed by transient urinary sodium excretion. The natriuretic threshold plasma ANP concentration during intravenous ANP infusion was 70-80 pmol/l. Atrial natriuretic peptide infused intra-arterially at a maximal forearm vasodilator dose (0.75 micrograms/min per 100 ml forearm tissue) increased forearm blood flow by 7.0 +/- 1.44 ml/min per 100 ml whereas the increase in sodium nitroprusside was 11.1 +/- 1.47 ml/min per 100 ml. Thus, ANP is rapidly released in response to atrial volume and pressure changes and represents a powerful vasodilating and, at high concentrations, natriuretic hormone in man.