心钠素31 - 67对集合管钠重吸收的调节作用。

Regulation of collecting duct Na+ reabsorption by ANP 31-67.

Zeidel M L

Laboratory of Epithelial Cell Biology, University of Pittsburgh Medical Center, PA 15213, USA.

Clin Exp Pharmacol Physiol. 1995 Feb;22(2):121-4. doi: 10.1111/j.1440-1681.1995.tb01967.x.

Abstract

The bulk of studies of the actions of atrial natriuretic peptides (ANP) have focussed on the carboxyterminal derivative (ANP 99-126) of the prohormone (ANP 1-126), but recent evidence indicates that an additional peptide derived from ANP 1-126, namely, ANP 31-67 also circulates, and has natriuretic actions. 2. The effects of ANP 31-67 on inner medullary collecting duct (IMCD) Na+ transport have been examined in freshly prepared suspensions of rabbit IMCD cells. Like ANP 99-126, ANP 31-67 reduces Na+ transport in these cells. 3. However, unlike ANP 99-126, this effect is not mediated by cGMP, and does not result from inhibition of apical Na+ channels. Rather, ANP 31-67 inhibits basolateral Na/K-ATPase, probably via the stimulation of PGE2 synthesis. 4. These results are discussed in the context of other natriuretic substances (interleukin 1 and endothelin), which also inhibit Na+ reabsorption by PGE2-mediated inhibition of Na/K-ATPase.

摘要

心房利钠肽（ANP）作用的大部分研究都集中在激素原（ANP 1-126）的羧基末端衍生物（ANP 99-126）上，但最近的证据表明，另一种源自ANP 1-126的肽，即ANP 31-67也在循环，并具有利钠作用。2. 已在新鲜制备的兔内髓集合管（IMCD）细胞悬液中研究了ANP 31-67对IMCD钠转运的影响。与ANP 99-126一样，ANP 31-67可减少这些细胞中的钠转运。3. 然而，与ANP 99-126不同，这种作用不是由环磷酸鸟苷（cGMP）介导的，也不是由顶端钠通道的抑制引起的。相反，ANP 31-67可能通过刺激前列腺素E2（PGE2）的合成来抑制基底外侧钠钾ATP酶。4. 这些结果在其他利钠物质（白细胞介素1和内皮素）的背景下进行了讨论，这些物质也通过PGE2介导的钠钾ATP酶抑制来抑制钠重吸收。