Transmembrane K Transfer in Hyperkalemic Dogs

Summary

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 transfers most of the infused K from extracellular to intracellular fluid. Treatment with β 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, β 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 β 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 β receptor blockade; if the hormone response is absent or deficient, β receptors may be importantly involved in mediation of K transfer to intracellular fluid.

Key-Words:

Hyperkalemia - Non-Renal K Homeostasis - Propranolol - β Adrenergic Receptor