The Effect of High Rates of Vasopressin Administration on Renal Potassium and Sodium Excretion During Potassium Loading in the Sheep

Abstract

1The influence of potassium loading on the renal excretion of sodium, potassium and solute during high rate vasopressin administration has been investigated in sheep.2 Adrenalectomized sheep were infused with 0.43 M KCI at 2 mI/min for 2-2.5 hours. Coincident with the rise in plasma potassium concentration, the urinary excretion of sodium, potassium, solute and water was increased as was the reabsorption of solute-free water. The rates of urinary excretion of sodium and potassium, osmolal clearance (Cosm) and solute-free water reabsorption (TCH20) for the first 50 min of potassium infusion were each found to be linearly related to the plasma potassium concentration. 3 After 50 min an infusion of vasopressin at 1 or 4 mu/min was superimposed on the potassium infusion for a period of 30 minutes. The administration of vasopressin was consistently associated with further augmentation of potassium excretion and clearance, of osmolal clearance and of solute-free water reabsorption to values above those anticipated from the pre-vasopressin regression lines for these parameters. Urinary sodium showed a coincident depression in the rate of excretion and clearance during the same period. 4 Thirty to fifty minutes after the cessation of vasopressin infusion the potassium and sodium excretions had returned to values which approximated the pre-vasopressin relations between plasma potassium and the urinary excretions of these ions. 5Both rates of vasopressin infusion were equally effective in increasing the potassium clearance. Any differences in clearance between the two rates of vasopressin administration were not statistically significant. 6 The large increments in potassium excretion (averaging > 40%) were interpreted as indicating that, when vasopressin is present at high concentrations, the distal tubule is one site of action of the hormone in the nephron of sheep.

Effects of vasopressin-glycine and vasopressin-glycine-lysine-arginine on renal function in the rat

“…How¬ ever, the extended peptides did not produce a sig¬ nificant natriuresis even at doses which were markedly antidiuretic. The mechanism of vasopressin-induced natriuresis is unknown; studies have ruled out a decrease in endogenous aldosterone release (Beai, 1976) or an indirect effect of the resultant volume expansion (Humphreys, Friedler & Earley, 1970). Vasopressin has been found to increase the backflux of sodium from the medullary interstitium into the collecting ducts (Tadokoro, Yamaguchi, Teruoka & Sakai, 1968;Ullrich, Baldamus, Uhlich & Rumrich, 1969) and this mechanism has also been postulated for prostaglandin-induced natriuresis (for review see Lote, 1982).…”