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大鼠肾上腺激素对肾外钾稳态的调节

Regulation of extrarenal potassium homeostasis by adrenal hormones in rats.

作者信息

Bia M J, Tyler K A, DeFronzo R A

出版信息

Am J Physiol. 1982 Jun;242(6):F641-4. doi: 10.1152/ajprenal.1982.242.6.F641.

DOI:10.1152/ajprenal.1982.242.6.F641
PMID:7046463
Abstract

The effect of chronic (7-10 days) adrenal insufficiency on extrarenal potassium tolerance was examined by infusing potassium into rats after acute nephrectomy. The increment in plasma potassium concentration was significantly higher in glucocorticoid-replaced adrenalectomized rats versus controls (max delta PK 3.59 +/-0.11 vs. 2.93 +/- 0.08 meq/liter; P less than 0.001). The impairment in extrarenal potassium tolerance in adrenalectomized rats could not be attributed to acidemia, hypotension, changes in plasma insulin or glucose concentration, or potassium retention prior to study. Acute replacement with aldosterone resulted in significant improvement in the rise in plasma potassium after KCl (max delta PK 3.18 +/- 0.06 meq/liter; P less than 0.005 compared with aldosterone-deficient adrenalectomized rats but higher than in controls, P less than 0.02). If given on a chronic basis, aldosterone replacement led to a complete correction of the defect (max delta PK = 2.89 +/- 0.08 meq/liter). Acute epinephrine replacement in adrenalectomized rats also returned potassium tolerance to normal (max delta PK = 3.02 +/- 0.10 meq/liter). The results demonstrate that extrarenal potassium tolerance is impaired in chronic adrenal insufficiency and suggest that both aldosterone and epinephrine deficiency may contribute to the defect, since replacement with either hormone returns potassium tolerance toward normal. Accordingly, both aldosterone and epinephrine have important extrarenal mechanisms of action.

摘要

通过在急性肾切除术后向大鼠输注钾,研究了慢性(7 - 10天)肾上腺功能不全对肾外钾耐受性的影响。与对照组相比,接受糖皮质激素替代的肾上腺切除大鼠血浆钾浓度的升高显著更高(最大ΔPK 3.59±0.11对2.93±0.08 meq/升;P<0.001)。肾上腺切除大鼠肾外钾耐受性的损害不能归因于酸血症、低血压、血浆胰岛素或葡萄糖浓度的变化,或研究前的钾潴留。急性给予醛固酮可显著改善氯化钾后血浆钾的升高(最大ΔPK 3.18±0.06 meq/升;与醛固酮缺乏的肾上腺切除大鼠相比,P<0.005,但高于对照组,P<0.02)。如果长期给予,醛固酮替代可完全纠正缺陷(最大ΔPK = 2.89±0.08 meq/升)。肾上腺切除大鼠急性给予肾上腺素也可使钾耐受性恢复正常(最大ΔPK = 3.02±0.10 meq/升)。结果表明,慢性肾上腺功能不全时肾外钾耐受性受损,提示醛固酮和肾上腺素缺乏均可能导致该缺陷,因为用任何一种激素替代均可使钾耐受性恢复正常。因此,醛固酮和肾上腺素均具有重要的肾外作用机制。

相似文献

1
Regulation of extrarenal potassium homeostasis by adrenal hormones in rats.大鼠肾上腺激素对肾外钾稳态的调节
Am J Physiol. 1982 Jun;242(6):F641-4. doi: 10.1152/ajprenal.1982.242.6.F641.
2
The effect of dexamethasone on renal potassium excretion and acute potassium tolerance.地塞米松对肾脏钾排泄及急性钾耐受性的影响。
Endocrinology. 1983 Nov;113(5):1690-6. doi: 10.1210/endo-113-5-1690.
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Extrarenal potassium homeostasis.肾外钾稳态
Am J Physiol. 1981 Apr;240(4):F257-68. doi: 10.1152/ajprenal.1981.240.4.F257.
4
Effect of insulinopenia and adrenal hormone deficiency on acute potassium tolerance.胰岛素缺乏和肾上腺激素缺乏对急性钾耐受性的影响。
Kidney Int. 1980 May;17(5):586-94. doi: 10.1038/ki.1980.69.
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Calcium channel blockers enhance extrarenal potassium disposal in the rat.钙通道阻滞剂可增强大鼠肾外钾的排泄。
Am J Physiol. 1986 Apr;250(4 Pt 2):F695-701. doi: 10.1152/ajprenal.1986.250.4.F695.
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Sympathetic system in potassium homeostasis.钾稳态中的交感神经系统。
Am J Physiol. 1981 Aug;241(2):F151-5. doi: 10.1152/ajprenal.1981.241.2.F151.
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Beta adrenergic control of extrarenal potassium disposal. A beta-2 mediated phenomenon.肾外钾排泄的β肾上腺素能调控。一种由β2介导的现象。
Nephron. 1986;43(2):117-22. doi: 10.1159/000183809.
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Parathyroid hormone impairs extrarenal potassium tolerance in the rat.甲状旁腺激素损害大鼠的肾外钾耐受性。
Am J Physiol. 1988 Mar;254(3 Pt 2):F385-90. doi: 10.1152/ajprenal.1988.254.3.F385.
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Extrarenal potassium adaptation: the role of aldosterone.
Clin Sci (Lond). 1989 Feb;76(2):213-9. doi: 10.1042/cs0760213.

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The effect of diuretics on extrarenal potassium tolerance.利尿剂对肾外钾耐受性的影响。
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Differential acute effects of aldosterone, dexamethasone, and hyperkalemia on distal tubular potassium secretion in the rat kidney.醛固酮、地塞米松和高钾血症对大鼠肾脏远曲小管钾分泌的急性差异作用。
J Clin Invest. 1984 Nov;74(5):1792-802. doi: 10.1172/JCI111598.
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Independent effects of aldosterone and potassium on induction of potassium adaptation in rat kidney.醛固酮和钾对大鼠肾脏钾适应诱导的独立作用。
J Clin Invest. 1987 Jan;79(1):198-206. doi: 10.1172/JCI112783.