Transmembrane K transfer in hyperkalemic dogs.

In a dog K loaded by infusion of 2 mEq KCl/kg/hr, kaluresis plays a relatively small part in slowing the development of hyperkalemia and cardiotoxicity. These are largely retarded by a non-renal mechanism that transfer most of the infused K from extracellular to intracellular fluid. Treatment with beta receptor blocking dosages of propranolol significantly reduces K transfer capacity, but it also markedly diminishes the KCl stimulated secretory response of insulin, a powerful mediator of K transfer. In dogs in which diminution of the insulin response is prevented by administration of exogenous hormone, beta receptor blockade has no effect on K transfer capacity. Thus, it appears that decreased insulin secretion is responsible for the observed fall of K transfer capacity in dogs with beta receptor blockade. However, other evidence suggests that our results can also mean that a K load elicits the secretion of enough insulin to mediate K transfer in the presence of beta receptor blockade; if the hormone response is absent or deficient, beta receptors may be importantly involved in mediation of K transfer to intracellular fluid.