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
