Insulin and beta receptor modulation of K homeostasis in nephrectomized dogs with hyperkalemia.
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. beta 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 beta 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 beta receptor blockade, nearly 90% is transferred. The results suggest that in the K homeostatic mechanism of nephrectomized dogs, insulin and beta receptors may be reciprocally related. K transfer mediated by beta receptors improves after pancreatectomy, and insulin mediated K transfer improves after beta receptors are inactivated.
D000450:Aldosterone / Q000502:physiology; D000818:Animals; D004285:Dogs; D005260:Female; D006706:Homeostasis; D006947:Hyperkalemia / Q000378:metabolism*; D007328:Insulin / Q000502:physiology*; D008297:Male; D009392:Nephrectomy; D011188:Potassium / Q000378:metabolism*; D011941:Receptors, Adrenergic / Q000502:physiology*; D011943:Receptors, Adrenergic, beta / Q000502:physiology*
D007328:Insulin; D011941:Receptors, Adrenergic; D011943:Receptors, Adrenergic, beta; D000450:Aldosterone; D011188:Potassium