Abstract

To study the relation between plasma atrial natriuretic peptide (ANP) and cardiac pressure, and to assess the pathophysiologic significance of ANP in water and electrolyte metabolism, the changes in plasma levels of ANP and arginine vasopressin (AVP) were examined in 11 patients with mitral stenosis who underwent percutaneous transvenous mitral valvuloplasty, and compared with the changes in the renin-angiotensin-aldosterone system and renal function. Immediately after valvuloplasty, plasma ANP levels decreased significantly with a concomitant decrease in mean pressures in the left atrium, the pulmonary artery and the right atrium. Plasma ANP levels decreased to the normal range in 4 of the 6 patients with normal sinus rhythm, while all 5 patients with atrial fibrillation had higher levels despite a similar degree of decrease in atrial pressure. There were significant positive correlations between plasma ANP levels and the mean left atrial pressure (r = 0.61, p < 0.01), the mean pulmonary arterial pressure (r = 0.49, p < 0.01) and the mean right atrial pressure (r = 0.54, p < 0.01). The mean plasma AVP levels, on the other hand, showed a transient increase after valvuloplasty from 0.5 ± 0.1 to 1.2 ± 0.4 pg/ml (p < 0.05). The mean plasma renin activity (1.3 ± 0.3 vs 2.7 ± 0.8 ng/ml/hr, p < 0.05) and plasma aldosterone concentration (8.6 ± 2.3 vs 17.2 ± 5.2 ng/dl, p < 0.05) also increased significantly 30 minutes a fter valvuloplasty. Further, a significant decrease in glomerular filtration rate (89 ± 7 vs 65 ± 5 ml/min, p < 0.01), renal plasma flow (435 ± 58 vs 305 ± 33 ml/min, p < 0.01), urine flow (2.3 ± 0.5 vs 1.0 ± 0.2 ml/min, p < 0.01) and urinary sodium excretion (162 ± 43 vs 73 ± 13 μmol/min, p < 0.05) was observed 30 minutes after valvuloplasty. These results suggest that (1) the cardiac atrium quickly responds to a reduction in atrial pressure to change its own ANP secretion, which directly or indirectly regulates water and sodium metabolism; (2) in addition to increased atrial pressure, bnormal atrial contraction per se stimulates ANP secretion; and (3) excessive AVP secretion leading to the postcommissurotomy syndrome is not linked to an abrupt reduction in atrial pressure itself.

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