Effect of vasodilator prostaglandins on the vascular renin-angiotensin system

Abstract

The interaction of prostaglandin (PG) with the vascular renin-angiotensin (R-A) system was examined by studies on the effects of PGI 2, PGE 2 and the inhibitor of PG synthesis, indomethacin, on the release of angiotensin II (Ang II) from isolated rat mesenteric arteries. The Ang II released from the vasculature was measured after its concentration in a Sep-Pak C 18 cartridge connected to the perfusion system. After perfusion with drugs, the specific vascular renin activity inhibited by anti-renin antibody was determined. The basal perfusion pressure was constant (19.6±1.1 mmHg at a flow rate of 4.5 ml/min, and was not changed by any of these drugs. The basal levels of Ang II release and vascular renin activity were 44 ± 5 pg/30 min and 113 ± 8 pg Ang I/mg protein /hr, respectively. Infusion of PGI 2 (10 −6 M) significantly decreased both Ang II release (p<0.01) and vascular renin activity (p<0.05) as compared with the control levels. Infusion of PGE 2 (10 −6 M) decreased Ang II release significantly (p<0.05) and vascular renin activity slightly. Infusion of indomethacin (10 −6M) increased vascular renin activity significantly (p<0.01). Pretreatment with indomethacin (10 mg/kg, ip) for 2 days also increased vascular renin activity (p<0.01). These results indicate that in contrast to their effects on the renal R-A system, PGs suppress the vascular R-A system and that these two local vasoactive factors interact to regulate vascular tone.