β Receptor Mediated Transfer in Potassium Loaded Nephrectomized Dogs

Abstract

Abstract

In nephrectomized dogs continuously infused with 2 mEq KCl/kg/hr, the development of hyperkalemia and cardiotoxicity is retarded by a homeostatic mechanism that transfers some 70% of the K load to intracellular fluid. Activity of the mechanism involves a β adrenergic receptor agonist since K transfer capacity is approximately halved by treatment with a blocking dosage of propranolol. The agonist is not endogenous epinephrine-adrenalectomy produces no change of K transfer ability; evidently an extraadrenomedullary agonist activates the β receptors involved in transport of a K load to intracellular fluid. Limiting blood flow to the brain by ligation of the cephalic arteries (an operation that elicits no immediate circulatory or cardiac impairment in dogs) also produces a significant fall of K transfer capacity; it is prevented by stimulating β receptors with epinephrine, i.e., combined with propranolol the hormone has no effect. The findings suggest that an extra adrenomedullary agonist of β receptors involved in K transfer is activated only if blood flow to the brain is unimpaired, since impairment, by ligation of cephalic arteries, results in a reduction of K transfer that is prevented by treatment with pharmacological dosages of epinephrine. Circulation in the cephalic arteries determines both blood flow and access of the K load to the brain. Thus it is possible that in nephrectomized dogs passage of K through the brain regulates activation of the β receptor agonist involved in K transfer.