title: 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.
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004285:Dogs; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D006339:Heart Rate; D007328:Insulin / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects / Q000502:physiology*; D008297:Male; D011188:Potassium / Q000378:metabolism*; D011433:Propranolol / Q000494:pharmacology
chemical_list: D007328:Insulin; D011433:Propranolol; D011188:Potassium; D004837:Epinephrine