Effects of neurohypophyseal antagonists in postnephrectomy natriuresis in male rats.

Abstract

Acute unilateral nephrectomy (AUN) in anesthetized male Lewis x DA rats induced rapid and consistent increases in electrolyte and fluid excretion by the remaining kidney during the first hours. Continuous infusion of a vasopressin (AVP) V1-receptor antagonist d(CH2)5Tyr(Me)AVP (V1-ant) reduced renal electrolyte and fluid excretion before and after AUN to a similar extent, whereas an oxytocin (OT)-receptor antagonist [Mpa1,D-Tyr(Et)2,Thr4,Orn8]-OT (CAP) at the same dose selectively attenuated the increase in sodium excretion after AUN. The plasma concentration of OT rose significantly after AUN (9.16 +/- 1.4 to 21.45 +/- 5.07 pg.ml-1). A similar OT level obtained by infusion of OT mimicked the renal responses to AUN without elevating blood pressure; however, only CAP but not V1-ant efficiently reversed OT-induced natriuresis. Also, the infusion of CAP at the same dose produced no effects on the rise of blood pressure caused by AVP while the infusion of the V1-ant prevented such a rise. Thus, CAP reduced the natriuresis after AUN by interfering with OT- and not V1-receptors. In conclusion, evidence is presented, for the first time, concerning the major role of OT receptors in the acute readjustment of the renal sodium excretion after AUN, and a synergistic role for AVP in terms of the general magnitude of renal excretion.