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醛固酮和膳食钾在大鼠远端结肠钾适应中的作用。

Role of aldosterone and dietary potassium in potassium adaptation in the distal colon of the rat.

作者信息

Foster E S, Jones W J, Hayslett J P, Binder H J

出版信息

Gastroenterology. 1985 Jan;88(1 Pt 1):41-6. doi: 10.1016/s0016-5085(85)80130-x.

Abstract

The present experiments were designed to differentiate the effects of aldosterone and chronic potassium loading in the mechanism of colonic potassium adaptation, using a recently described animal model that permits systematic manipulation of aldosterone and dietary potassium. Unidirectional 42K fluxes were performed under short-circuit conditions across isolated distal colonic mucosa from rats with intact adrenal glands and in adrenalectomized, hormone-replaced animals. Administration of a potassium-enriched diet reversed net potassium absorption (+0.43 +/- 0.10 muEq/h.cm2) in intact animals to net potassium secretion (-0.76 +/- 0.08 muEq/h.cm2). Infusion of aldosterone in adrenalectomized animals, in an amount equivalent to that produced by potassium loading in intact rats, reduced JnetK to zero (-0.03 +/- 0.06 muEq/h.cm2). Similarly, zero net potassium transport (-0.14 +/- 0.08 muEq/h.cm2) was observed when experimental rats were fed a potassium-enriched diet and maintained with basal aldosterone levels. Therefore, both elevated aldosterone levels and a potassium-enriched diet had an effect on net potassium transport, but neither produced the full effects of chronic potassium loading. An increase in net potassium secretion (-0.57 +/- 0.07 myEq/h.cm2) comparable to that of intact potassium-loaded animals did, however, occur when potassium loading and elevated aldosterone levels were combined in experimental animals. These studies demonstrate that (a) chronic potassium loading alters active potassium transport by an aldosterone-independent mechanism and (b) the mechanism of chronic potassium adaptation represents the additive effects of increased dietary potassium and aldosterone.

摘要

本实验旨在利用一种最近描述的动物模型来区分醛固酮和慢性钾负荷在结肠钾适应性机制中的作用,该模型允许对醛固酮和饮食钾进行系统调控。在短路条件下,对来自肾上腺完整大鼠以及肾上腺切除并接受激素替代的动物的离体远端结肠黏膜进行单向(42K)通量测定。给予富含钾的饮食可使完整动物的钾净吸收((+0.43\pm0.10)微当量/小时·平方厘米)转变为钾净分泌((-0.76\pm0.08)微当量/小时·平方厘米)。给肾上腺切除的动物输注醛固酮,其量相当于完整大鼠钾负荷所产生的量,可使钾净通量((JnetK))降至零((-0.03\pm0.06)微当量/小时·平方厘米)。同样,当给实验大鼠喂食富含钾的饮食并维持基础醛固酮水平时,观察到钾净转运为零((-0.14\pm0.08)微当量/小时·平方厘米)。因此,醛固酮水平升高和富含钾的饮食均对钾净转运有影响,但两者均未产生慢性钾负荷的全部效应。然而,当在实验动物中同时进行钾负荷和醛固酮水平升高时,出现了与完整钾负荷动物相当的钾净分泌增加((-0.57\pm0.07)毫当量/小时·平方厘米)。这些研究表明:(a)慢性钾负荷通过一种不依赖醛固酮的机制改变钾的主动转运;(b)慢性钾适应性机制代表了饮食钾增加和醛固酮的叠加效应。

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