Metzler C H, Gardner D G, Keil L C, Baxter J D, Ramsay D J
Am J Physiol. 1987 Jan;252(1 Pt 2):R188-92. doi: 10.1152/ajpregu.1987.252.1.R188.
The escape from the sodium-retaining effects of prolonged mineralocorticoid treatment in animals and humans was first noted over 40 yr ago, but despite intense study the mechanisms responsible for the escape phenomenon have not been identified. Putative "natriuretic hormones" have been proposed to account for the escape phenomenon. To determine whether atrial natriuretic peptides (ANP) could participate in the escape phenomenon, the mineralocorticoid deoxycorticosterone acetate (DOCA) was administered to conscious dogs for 14 days. Escape was accompanied by a doubling of plasma ANP concentration and four- to sevenfold increases in cardiac ANP messenger RNA. There were also significant increases in mean arterial blood pressure during the last 8 days of DOCA treatment. Thus increases in the synthesis and secretion of ANP and increases in atrial pressure may represent mechanisms that contribute to the escape from mineralocorticoid-induced sodium retention.
40多年前人们首次注意到，动物和人类在长期接受盐皮质激素治疗后会摆脱钠潴留效应，但尽管进行了深入研究，导致这种逃逸现象的机制仍未明确。有人提出假定的“利钠激素”来解释这种逃逸现象。为了确定心房利钠肽（ANP）是否参与逃逸现象，给清醒的犬注射盐皮质激素醋酸脱氧皮质酮（DOCA），持续14天。逃逸过程伴随着血浆ANP浓度翻倍以及心脏ANP信使核糖核酸增加4至7倍。在DOCA治疗的最后8天，平均动脉血压也显著升高。因此，ANP合成和分泌的增加以及心房压力的升高可能是导致摆脱盐皮质激素诱导的钠潴留的机制。
