Studies on the effects of viprostol in isolated small blood vessels and thoracic aorta of the rat

Abstract

1 The effects of viprostol, prostaglandin E2 (PGE2) and nitroglycerin were studied in basilar artery, small mesenteric artery and the vein parallel to it as well as thoracic aorta of the rat. 2 In KCl-contracted basilar artery, viprostol produced a concentration-related biphasic response, contraction at concentrations <3 x 10-6 M and relaxation at concentrations >3 x 10-6 M. PGE2 produced a concentration-related contraction while nitroglycerin produced a concentration-related relaxation. 3 In KCI-contracted small mesenteric artery, viprostol produced a biphasic response which was similar to that in the basilar artery. PGE2 produced a contraction and nitroglycerin produced relaxation in a concentration-dependent manner. 4 In KCl-contracted small mesenteric vein, in contrast to basilar and mesenteric artery, viprostol produced only a concentration-related relaxation in the range of 1 x 10-6 to 1 x 10-4 M. PGE2 produced a contraction and nitroglycerin produced a concentration-related relaxation. 5 In KCl-contracted thoracic aorta, PGE2 produced a biphasic response, relaxation at concentrations < 3 x 10-7 M and a concentration-related contraction at concentrations > 3 x Il0-M. Viprostol only produced a concentration-related contraction at concentrations > 1 x 106 M, which was significantly less in magnitude than the contraction produced by PGE2. Nitroglycerin produced a concentration-related relaxation as seen in the small vessels. 6 In conclusion, the present data demonstrate that viprostol is a vasorelaxant agent which effectively dilates KCl-contracted basilar, small mesenteric artery and vein, but not the thoracic aorta of rat. The potent antihypertensive action of viprostol is probably due to its relaxant effect on the small arteries and veins but not on the large conduit artery.

The release of a non‐prostanoid inhibitory factor from rabbit bronchus detected by co‐axial bioassay

“…Although mepacrine and NDGA are relatively non-specific in effect (Griffith et al, 1984), no inhibition was observed. Furthermore, prostaglandin E2 contracts rat endothelium-denuded aorta (Lai et al, 1988) and LTC4, LTD4 and LTE4 also failed to relax this preparation (this study). Haemoglobin and phenidone, inhibitors of EDRF (Griffith et al, 1984;Martin et al, 1985) and gossypol, an inhibitor of EDRF synthesis and/or release (Forstermann et al, 1986) at concentrations known to inhibit EDRF (also confirmed in this study), failed to inhibit relaxation induced by methacholine.…”