Insulin and β Receptor Modulation of K Homeostasis in Nephrectomized Dogs with Hyperkalemia

Summary

In nephrectomized dogs infused with 2 mEq KCl/kg/hr a homeostatic mechanism retards the development of hyperkalemia by transferring about 70% of the K load to intracellular fluid. β Adrenergic receptor activity is importantly involved in the transfer process; halting it with propranolol reduces the proportion transferred to less than 35%. The addition of pancreatectomy increases the involvement of β receptor activity; propranolol treatment now reduces the proportion transferred to less than 20%. Insulin treatment, on the other hand, not only improves transfer of a K load, it also alters the response to propranolol. Nephrectomized dogs treated with 2 U insulin/kg/hr deposit some 80% of the infused K in intracellular fluid. After β receptor blockade, nearly 90% is transferred. The results suggest that in the K homeostatic mechanism of nephrectomized dogs, insulin and β receptors may be reciprocally related. K transfer mediated by β receptors improves after pancreatectomy, and insulin mediated K transfer improves after β receptors are inactivated.

Key-Words:

Nephrectomy - Dogs - Hyperkalemia - K Homeostasis - β Adrenergic Receptors - Propranolol - Insulin