In vivo influence of prostaglandin I2 on systemic and renal circulation in the rat.

The effect of prostaglandin I2 and two other vasodilator agents, acetylcholine and sodium nitroprusside, on systemic and renal circulation was studied in 29 adult euvolemic Sprague-Dawley rats. Intra-aortic infusion of prostaglandin I2 (3.6 micrograms/kg/hr; n = 6 rats) produced significant vasodilation (p less than 0.05), as indicated by an average reduction in total peripheral vascular resistance of 24.8 +/- 2.0%, while renal vascular resistance remained essentially unchanged. Essentially identical findings were obtained in a separate group of six rats pretreated with intravenous administration of saralasin (0.5 mg/kg/hr). In contrast, in another group of six rats pretreated with saralasin, intraaortic infusion of acetylcholine (0.35 mg/kg/hr), which caused a reduction in total peripheral vascular resistance (21.4 +/- 3.8%) comparable to that induced by prostaglandin I2, produced a significant fall in renal vascular resistance (average, 27.7 +/- 5.0%) and, hence, an increase in renal blood flow (average, 26.2 +/- 2.9%). The effect of sodium nitroprusside (0.4 mg/kg/hr i.v.) was intermediate between those of prostaglandin I2 and acetylcholine: both renal vascular resistance and total peripheral vascular resistance fell mildly. These results indicate that prostaglandin I2, given in a dose sufficient to cause systemic vasodilation, fails to induce any discernible renal vasodilative response and that this absence of renal vasodilation by prostaglandin I2 in vivo is not due, as previously postulated, to the highly efficient offsetting influence of intrarenal angiotensin II release.