In ureter ligated dogs intravenous administration of KCI stimulates both insulin secretion and activity of a kaluresis independent K homeostatic mechanism (K transfer capacity) that retards the development of hyperkalemia by transferring K to intracellular fluid. If the preparation is K loaded by infusion with 2 mEq KCI/kg/hr until prelethal ECG changes of hyperkalemic cardiotoxicity appear, about 50% of administered K is transferred. An increased proportion - 70% - is transferred if the animal is K loaded 70 minutes after pancreatectomy - when serum immunoreactive insulin is fixed at < 4 uU/ml. That proportion (70%) is unchanged by simultaneous adrenalectomy, but is reduced to less than 40% by propranolol blockade of B receptors. Increased post pancreatectomy K transfer capacity apparently involves K transfer mediated by B receptors that are activated by an extra-adrenomedullary B agonist(s). Findings also indicate that residual post pancreatectomy insulin biological activity mediates K transfer.
Hyperkalemia
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B Receptor Blockade
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K Transfer Capacity
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Insulin Biological Activity
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Adrenalectomy
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Extra-Adrenal B Agonist
