Regulation of rat renal alpha 2 B-adrenergic receptors by potassium depletion.
Regulation of rat renal alpha 2 B-adrenergic receptors by potassium depletion.
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通过钾消耗调节大鼠肾α2B-肾上腺素能受体。
DOI：
10.1152/ajprenal.1994.266.2.f316
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Okusa,MD
中科院分区：
文献类型：
--
作者：
Muir,JC;Huang,L;Harrison,JK;Rosin,DL;Okusa,MD
Potassium depletion and alpha 2-adrenergic receptor (alpha 2-AR) agonists produce similar physiological effects on renal function. Both stimuli increase Na-H exchange in proximal tubule cells, inhibit water transport in collecting tubule cells, and alter blood pressure regulation. The purpose of this study was to determine whether potassium depletion and renal alpha 2-AR subtype expression were linked. Kidney membrane proteins and RNA were harvested from anesthetized rats fed a potassium-deficient diet for 4-20 days (LK 4 to LK 20). Using a selective alpha 2-AR antagonist, [3H]MK-912, we observed that potassium depletion led to a dramatic increase in maximum binding (270% of control) without a change in dissociation constant. Competitive binding studies in LK 14 kidney membranes employing chlorpromazine, prazosin, and oxymetazoline suggested that the increase in alpha 2-ARs in response to potassium depletion was due primarily to an increase in the B subtype of alpha 2-AR. Northern blot analysis demonstrated that renal alpha 2B-AR mRNA levels increased (190% of control) after 4 or 14 days on a potassium-deficient diet. In contrast, there was no difference in steady-state alpha 2A-receptor protein levels by Western blot analysis. We conclude that potassium depletion selectively increases the expression of the B subtype of alpha 2-AR with no detectable effect on alpha 2A-AR expression.
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DOI：
10.1016/s0021-9258(19)70664-4
发表时间：
1980
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
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影响因子：
2.9
作者：
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通讯作者：
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影响因子：
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作者：
J. L. Tymoczko;M. M. Phillips;S. Vernon
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DOI：
10.1016/0022-4731(85)90140-2
发表时间：
1985
期刊：
Journal of steroid biochemistry
影响因子：
--
作者：
G. Rossini
通讯作者：
G. Rossini
影响因子：
3.5
作者：
ECONOMIDIS, IV;ROUSSEAU, GG
通讯作者：
ROUSSEAU, GG