Atriopeptin II lowers cardiac output in conscious sheep

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Abstract
Atrial natriuretic peptides cause natriuresis, kaliuresis, diuresis, and hypotension. They relax vascular smooth muscle in vitro, and they dilate renal vessels in vivo. Hence, we tested the hypothesis that they produce hypotension by lowering total peripheral resistance. The studies were performed in conscious chronically instrumented sheep standing quietly in their cages. Atriopeptin II (AP II) was infused into the right atrium for 30 min at 0.1 nmol .cntdot. kg-1 .cntdot. min-1. Atriopeptin II lowers arterial pressure (9%, P < 0.05) by lowering cardiac output (81%, P < 0.05), stroke volume (28%, P < 0.05), and right atrial pressure (2.3 mmHg, P < 0.05). Heart rate and total peripheral resistance increase (16 and 13%, respectively, P < 0.05). Partial ganglionic blockade with trimethaphan camsylate during AP II infusion prevents the increaes in heart rate and total peripheral resistance. The changes in right atrial pressure, stroke volume, and cardiac output persist, and arterial pressure falls further (27%, P < 0.05). These hemodynamic data are consistent with direct AP II-induced relaxation of venous smooth muscle with reduction of venous return, right atrial pressure, stroke volume, cardiac output, and arterial pressure, followed by reflex activation of the sympathetic nervous system to increase heart rate and total peripheral resistance. Because partial ganglionic blockade alone and AP II alone cause similar reductions in right atrial pressure (2.1 and 2.3 mmHg, respectively) but AP II causes a greater fall in stroke volume (28 vs. 13%), it is possible that AP II also causes coronary vasoconstriction.

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