Transmembrane K Transfer in Hyperkalemic Dogs

Abstract

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.

Kaluresis Independent K-Homeostasis: Glucagon and B Receptor Blockade in Pancreatectomized Dogs

“…In dogs K loaded 70 minutes post pancx serum IRI is fixed at < 4 uU/ml and K transfer capacity is ample -more than 2/3 NK is transferred to ICF (Table 2, Group I). Treatment with either a B receptor blockading dosage of propranolol ( Insulin and B receptors are the most important mediators of transmembrane K transfer in K loaded dogs (Hiatt et al 1981). In nephrectomized (nephx) preparations they are reciprocally related.…”

Hyperkalemia and the electrocardiogram in dogs

“…the impending onset of ventricular fibrillation (1). In the present investigation dogs were rapidly infused with KCI and serum K concentration of coronary artery blood was measured.…”