Abstract
Urotensin I (UI) elicits dose-dependent relaxation responses in isolated helical strips of rat tail and mesenteric arteries contracted by 10 −5M norepinephrine (NE). The rat mesenteric artery demonstrated a 40 fold lower threshold sensitivity to UI (0.25 mU/M1 versus maximal relaxation at 0.25 mU/m1). Complete relaxation of the rat tail artery with UI could not be achieved, even at doses exceeding 10 mU/m1. Pretreatment of the arterial strips with cyclooxygenase inhibitors had no effect on the contractile response to NE in the tail artery, but reduced NE responsiveness in the mesenteric artery. Significant enhancement of UI relaxation responses in both types of arterial strips was achieved by pre-treatment with the cyclooxygenase inhibiters, suggesting a modulatory role for prostaglandins (PGs) in the expression of the UI relaxation response in NE contracted arterial strips. The major enzymatically formed PG (as assessed by [1- 14C] PGH 2 metabolism in broken cell preparations) in both the rat tail and mesenteric arteries was 6-keto PGF 1α, the stable hydrolysis product of PGI 2. Using a specific RIA to quantify 6-keto PGF 1α release, it was found that UI elicited nearly a two-fold increase in the release of this PG compared to the NE control in both rat tail and mesenteric arteries. These data suggest that PGI 2 may modulate the relaxation response to UI either by direct physiological opposition (PGI 2 elicited contractile response in NE contracted tail and mesenteric arteries at doses exceeding 10−8M) and/or by some as yet undefined mechanism (eg. effects on Ca 2+, cAMP).
Published Version
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