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

Regulation of amiloride-sensitive electrogenic sodium transport in the rat colon by steroid hormones.
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类固醇激素对大鼠结肠中阿米洛利敏感的电化学钠转运的调节。

DOI:
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发表时间:
1985
影响因子:
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通讯作者:
U. Hopfer
U. Hopfer
中科院分区:
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文献类型:
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作者:
P. Will;R. Cortright;R. DeLisle;J. Douglas;U. Hopfer

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本研究通过向肾上腺切除(ADX)大鼠体内注入类固醇并测定离体结肠短路电流(ISC),探讨了类固醇在结肠钠转运中的作用。醛固酮和皮质酮分别以2和260 μ g × kg ~(-1)× h ~(-1)的半数最大剂量(ED_(50))诱导阿米洛利敏感性ISC。合成糖皮质激素如甲基强的松龙(33 mg/kg)和地塞米松(ED 50 = 30 μ g X kg-1 X h-1)也有效。超最大剂量的醛固酮(7.5倍ED 50)24小时增加总ISC(7倍),阿米洛利敏感的ISC(366倍),电导(2倍),以及钾刺激的磷酸酶活性(2倍)(先前报道)。与醛固酮相比,超最大剂量的地塞米松(4倍ED 50)产生更大的增加总ISC(15倍)和阿米洛利敏感的ISC(674倍)。与醛固酮相比,地塞米松也增加了阿米洛利不敏感的ISC(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被地塞米松增加到与非糖尿病大鼠相似的程度(11倍)。雌二醇、孕酮和睾酮对ADX大鼠结肠ISC无刺激作用。根据阿米洛利敏感性钠转运测定的皮质酮和醛固酮的ED 50值,产生的血清水平略高于未受应激的肾上腺完整动物的血清水平,因此必须认为是生理性的。可以得出结论,在生理水平的类固醇可以介导阿米洛利敏感的钠转运在大鼠结肠。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剂。
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.