Role of prostacyclin in the renal response to acetylcholine.

Abstract

Renal arterial infusion of acetylcholine (ACh; 40 micrograms/min) in control dogs produced a sustained rise in urinary sodium excretion (UNa V) and in renal plasma flow (RPF). When prostaglandin (PG) synthesis was inhibited with indomethacin (5 mg/kg), ACh produced only a transient rise in UNa V and RPF followed by a progressive decline in UNa V and RPF. Renal arterial infusion of PGI2 (0.2 microgram/min) restored the response to ACh to normal in indomethacin-treated dogs. The RPF was 84 +/- 9 ml/min during control and increased to 132 +/- 19 ml/min with the infusion of PGI2 (p < 0.01). RPF increased further to 188 +/- 18 ml/min at 20-min infusion of ACh and was maintained at 189 +/- 14 ml/min at 100-min infusion of ACh (p < 0.01). Our data suggest that the initial rise in RPF by ACh is independent of the PG system, whereas maintenance of the rise in RPF by ACh requires an intact synthesis of PGs, presumably PGI2 synthesized in the vascular tissues.