Greenwald J E, Sakata M, Michener M L, Sides S D, Needleman P
Department of Pharmacology, Washington University School of Medicine, St. Louis, Missouri 63110.
J Clin Invest. 1988 Apr;81(4):1036-41. doi: 10.1172/JCI113414.
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.
心房肽（AP）是一种具有利钠、利尿和血管舒张作用的肽，由哺乳动物心房合成并分泌。该肽在心血管生理和病理生理中的明确作用尚未确定。我们培育了一群对自身AP致敏的自身免疫性大鼠，以评估长期AP缺乏对生理和病理生理过程的影响。自身免疫性大鼠对急性静脉容量扩张的利钠反应受到抑制，然而，这些动物经慢性口服盐负荷产生的利钠作用并未受到抑制。当将血浆AP作为血压的函数进行评估时，自发性高血压大鼠的血浆AP增加了三倍。与未免疫的对照组相比，对这些大鼠进行免疫对其高血压的发展速度、发展中的高血压程度或其每日钠排泄量均无影响。在给大鼠注射醋酸脱氧皮质酮期间发生了盐皮质激素逃逸现象。大鼠从这种类固醇的保钠作用中逃逸的能力不受先前针对AP免疫的影响。这些结果表明，AP是对急性血管内容量负荷作出反应的一种重要利钠物质。然而，心房肽似乎不参与对慢性血管内容量负荷的利钠反应、血压调节或盐皮质激素逃逸。
