Renal hemodynamic responses to intrarenal infusion of acetylcholine: Comparison with effects of PGE2 and NO donor

Acetylcholine ( Ach) could serve as a selective renal medullary vasodilator in studies of the mechanism of arterial pressure regulation; however, effects of intramedullary Ach infusion were disparate. In anesthetized rats, the total renal blood flow ( RBF) was measured by renal artery probe, and local perfusion of the cortex ( CBF), outer medulla ( OMBF) and inner medulla ( IMBF) as laser-Doppler ( I-D) flux. Renal artery infusion of Ach ( 60-150 mu g/kg/h) significantly increased RBF by 17% and I-D parameters by 7-14%, without affecting arterial blood pressure ( BP); the responses were prevented by inhibition of nitric oxide ( NO) synthesis with N-omega-nitro-L-arginine methyl ester ( L-NAME). Intramedullary Ach ( 180 mu g/kg/h) significantly increased OMBF by 9% and IMBF by 7% but also RBF and CBF ( both 9%). Carbamylcholine ( Cch, 15 or 30-60 mu g/kg/h), a stable Ach analog, increased CBF, OMBF, and IMBF by 5-8%; there was no dose dependency and, as with Ach, no preferential effect on medullary perfusion. Intramedullary infusion of prostaglandin E-2 ( PGE2) ( 15 mu g/kg/h), and S-nitroso-N-acetyl-D, L penicillamine ( SNAP), an NO donor ( 15-30mg/kg/h), significantly and substantially increased OMBF and IMBF only. Ach increased perfusion of all kidney zones by an NO-dependent mechanism. Infusion of Ach or Cch into the renal medullary interstitium failed to affect preferentially the medullary perfusion, in contrast to the well-demonstrable selective effects of PGE2 and SNAP. The reason was probably the Ach's dual opposed action, vasoconstrictor and vasorelaxant, on the intrarenal vasculature.