Abstract
Atriopeptin (AP), a natriuretic-diuretic and vasodilatory peptide, is synthesized and secreted from mammalian atria. The definitive role of this peptide on cardiovascular physiology and pathophysiology has yet to be determined. We developed a population of autoimmune rats sensitized against their own AP to evaluate the consequences of prolonged AP deficiency on physiological and pathophysiological processes. Natriuresis in response to acute intravenous volume expansion was inhibited in the autoimmune rat, however, natriuresis produced by chronic oral salt loading was not suppressed in these animals. Plasma AP increased threefold in the spontaneously hypertensive rat when evaluated as a function of blood pressure. Immunization of these rats had no effect on the rate of development, magnitude of their developing hypertension, or their daily sodium excretion when compared with nonimmunized controls. Mineralocorticoid escape occurred during desoxycorticosterone acetate administration to rats. The ability of rats to escape from the sodium-retaining effects of this steroid was not affected by prior immunization against AP. These results suggest that AP is an important natriuretic substance in response to acute intravascular volume loading. However, atriopeptin does not appear to be involved in the natriuretic response to chronic intravascular volume loading, blood pressure regulation, or mineralocorticoid escape.
Authors
J E Greenwald, M Sakata, M L Michener, S D Sides, P Needleman
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