Neural Factor in K Homeostasis of Hyperkalemic Ureter-Ligated Dogs

Abstract

Abstract

In ureter ligated or nephrectomized dogs continuously infused with 2 mEq KCl/kg/hr, a nonrenal K homeostatic mechanism retards the development of hyperkalemia by transferring much of the K load from extracellular to intracellular fluid. But, the K transfer capacity of ureter-ligated dogs is significantly less than that of equally anuric nephrectomized animals. However, K transfer ability in ureter-ligated dogs can be raised to the nephrectomy level if the kidneys are denervated or if the animals are vagotomized by cutting both cervical vagus trunks; in ureter-ligated preparations with bilateral adrenalectomy, vagotomy is without effect. It has been shown that in anuric dogs activity of β-adrenergic receptors is importantly involved in transfer of a K load to intracellular fluid. Our findings suggest that ureter-ligated kidneys give rise to neural impulses that course in fibers of the cervical vagus trunk and diminish K transfer by suppressing the secretion of epinephrine, a powerful β receptor agonist that is known to increase K transfer markedly in these preparations. Division of the renal nerves or of the vagus trunks in the neck interrupts the inhibiting neural impulses and releases secretion of endogenous hormone, with a corresponding rise of K transfer; unless the source of epinephrine is removed by adrenalectomy.