The ability to dispose of an acute intravenous potassium load was examined in glucocorticoid-replaced adrenalectomized rats and in rats made insulinopenic with somatostatin. Adrenalectomy resulted in a significantly greater rise in plasma potassium concentration compared with controls (1.46 ± 0.11 vs. 0.92 ± 0.05 mEq/l, P < 0.001) despite the excretion of an identical percentage (47%) of the administered potassium load in 2 hr. Somatostatin-induced insulinopenia (insulin levels decreased from 37 ± 5 to 20 ± 3 μU/ml) was also associated with a significantly greater increment in plasma potassium concentration (1.51 ± 0.20 mEq/l, P < 0.001) compared with controls, despite the excretion of a similar amount (39%) of the administered potassium load. In animals with combined adrenal and insulin deficiency, the rise in plasma potassium concentration occurred earlier and remained elevated for a more prolonged period of time compared with animals with either adrenalectomy or insulinopenia alone. Conclusion. During acute potassium loading in the rat, insulin and adrenal hormones play an important role in maintaining normal potassium homeostasis, primarily by enhancing potassium uptake by extrarenal tissues.
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