Wambach G, Götz S, Suckau G, Kaufmann W
Klin Wochenschr. 1986;64 Suppl 6:53-7.
A natriuretic factor has long been postulated to play a role in renal mineralocorticoid escape. We therefore investigated changes in plasma levels of atrial natriuretic peptide (ANP) during chronic treatment with 9 alpha-fluorohydrocortisone. Five normal subjects were studied on a constant diet (300 meq Na+ and 72 meq K+ per day) and received 0.8 mg 9 alpha-fluorohydrocortisone for up to 14 days. Sodium balance became positive and body weight increased between 1.0-4.5 kg maximally. Serum aldosterone was suppressed and plasma levels of ANP were stimulated up to 10-fold. Increment in plasma ANP was positively correlated with the gain in body weight (r = 0.666, p less than 0.001). Renormalization of sodium balance was seen in two subjects, however the maximum in plasma ANP did not occur during the time of renal escape. ANP-secretion is stimulated during sodium retention induced by mineralocorticoids, however ANP does not seem to trigger the escape mechanism.
长期以来,人们一直推测利钠因子在肾盐皮质激素脱逸中起作用。因此,我们研究了在使用9α-氟氢可的松进行慢性治疗期间心房利钠肽(ANP)血浆水平的变化。对5名正常受试者进行了研究,他们保持恒定饮食(每天300毫当量钠和72毫当量钾),并接受0.8毫克9α-氟氢可的松治疗长达14天。钠平衡变为正值,体重最大增加1.0 - 4.5千克。血清醛固酮受到抑制,ANP血浆水平升高至原来的10倍。血浆ANP的增加与体重增加呈正相关(r = 0.666,p < 0.001)。两名受试者的钠平衡恢复正常,然而血浆ANP的最大值并非出现在肾脱逸期间。在盐皮质激素诱导的钠潴留期间,ANP分泌受到刺激,然而ANP似乎并未触发脱逸机制。