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类固醇激素对大鼠结肠中阿米洛利敏感的生电钠转运的调节。

Regulation of amiloride-sensitive electrogenic sodium transport in the rat colon by steroid hormones.

作者信息

Will P C, Cortright R N, DeLisle R C, Douglas J G, Hopfer U

出版信息

Am J Physiol. 1985 Jan;248(1 Pt 1):G124-32. doi: 10.1152/ajpgi.1985.248.1.G124.

DOI:10.1152/ajpgi.1985.248.1.G124
PMID:3966555
Abstract

The role of steroids in the regulation of colonic sodium transport was examined by infusing steroids into adrenalectomized (ADX) rats and evaluating the short-circuit current (ISC) in vitro. Amiloride-sensitive ISC was induced by aldosterone and corticosterone with half-maximal doses (ED50) of 2 and 260 micrograms X kg-1 X h-1), respectively. Synthetic glucocorticoids such as methylprednisolone (33 mg/kg) and dexamethasone (ED50 = 30 micrograms X kg-1 X h-1) were also effective. Supramaximal doses of aldosterone (7.5 times ED50) for 24 h increased the total ISC (7-fold), the amiloride-sensitive ISC (366-fold), and the conductance (2-fold), as well as the potassium-stimulated phosphatase activity (2-fold) (reported previously). Compared with aldosterone, supramaximal doses of dexamethasone (4 times ED50) produced greater increases in the total ISC (15-fold) and the amiloride-sensitive ISC (674-fold). In contrast to aldosterone, dexamethasone also increased the amiloride-insensitive ISC (3-fold). Glucocorticoid action was not mediated by insulin since the ISC from diabetic ADX rats was increased by dexamethasone to a similar extent (11-fold) as in nondiabetic rats. Estradiol, progesterone, and testosterone did not stimulate the colonic ISC of ADX rats. The ED50 values of corticosterone and aldosterone, measured in terms of amiloride-sensitive sodium transport, produced serum levels that were slightly above those of unstressed, adrenal-intact animals and thus must be considered physiological. It is concluded that at physiological levels both steroids may mediate amiloride-sensitive sodium transport in the rat colon. However, as judged from changes in serum steroid levels, aldosterone is the physiological regulator of elevated sodium absorption in sodium deficiency.

摘要

通过向肾上腺切除(ADX)大鼠输注类固醇并在体外评估短路电流(ISC),研究了类固醇在结肠钠转运调节中的作用。醛固酮和皮质酮可诱导阿米洛利敏感的ISC,其半数最大剂量(ED50)分别为2和260微克·千克⁻¹·小时⁻¹。合成糖皮质激素如甲泼尼龙(33毫克/千克)和地塞米松(ED50 = 30微克·千克⁻¹·小时⁻¹)也有效。醛固酮超最大剂量(7.5倍ED50)持续24小时可使总ISC增加7倍、阿米洛利敏感的ISC增加366倍、电导增加2倍,以及钾刺激的磷酸酶活性增加2倍(先前已报道)。与醛固酮相比,地塞米松超最大剂量(4倍ED50)可使总ISC增加15倍、阿米洛利敏感的ISC增加674倍。与醛固酮相反,地塞米松还可使阿米洛利不敏感的ISC增加3倍。糖皮质激素的作用不是由胰岛素介导的,因为糖尿病ADX大鼠的ISC被地塞米松增加的程度(11倍)与非糖尿病大鼠相似。雌二醇、孕酮和睾酮不会刺激ADX大鼠的结肠ISC。根据阿米洛利敏感的钠转运测量的皮质酮和醛固酮的ED50值产生的血清水平略高于未受应激、肾上腺完整动物的水平,因此必须被视为生理水平。结论是,在生理水平上,两种类固醇都可能介导大鼠结肠中阿米洛利敏感的钠转运。然而,从血清类固醇水平的变化判断,醛固酮是钠缺乏时钠吸收增加的生理调节因子。

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