Rat renal hemodynamics during venous compression: roles of nerves and prostaglandins.

Experiments were conducted on euvolemic rats to characterize renal hemodynamic responses to a unilateral increase in renal venous pressure. Ipsilateral renal blood flow (RBF, electromagnetic flow probe) was measured in four groups to determine the roles of the renal nerves and endogenous prostaglandins. In control rats, elevation of venous pressure (3 to 22 mmHg) produced vasoconstriction and a 16% increase in renal vascular resistance (RVR) at 130 mmHg arterial pressure (P less than 0.001). In acutely denervated kidneys, a 19-mmHg increase in venous pressure reduced RBF but did not alter RVR (5% decrease), since there were proportional decreases in RBF and the arteriovenous pressure gradient. Indomethacin-treated rats with innervated kidneys responded to a similar increase in venous pressure with pronounced constriction; RVR increased by 50% (P less than 0.005). Venous compression elicited a 24% increase in RVR (P less than 0.05) in indomethacin-treated rats with denervated kidneys. The opposing effects of denervation and indomethacin treatment were significant and noninteractive. The findings indicate 1) activation of an ipsilateral renorenal neural reflex mediated a significant portion of the vasoconstriction; and 2) enhanced synthesis of prostaglandins produced net dilatory effects that attenuated the neurally mediated constriction. The opposing actions of the renal nerves and prostaglandins on the RVR responses to increased venous pressure were directly related to arterial pressure between 70 and 130 mmHg. In response to decrements in arterial pressure, the general pattern of vasodilation was not impaired by denervation of indomethacin when venous pressure was normal or elevated. These observations indicate that the origin of the pressure change, i.e., arterial vs. venous, engages different vasoactive factors that are responsible for varying circulatory responses in the rat kidney.