Effects of prostaglandins E1, E2, A1, and F1-alpha on isolated vascular smooth muscle

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Abstract
Prostaglandin E compounds are potent vasodepressors in situ, decreasing blood pressure and vascular resistance. Parodoxically, they cause contraction of isolated aortic strips in vitro. This study explores the effects of prostaglandins E1, E2, A1 (PGE1-217), and F1[alpha] on isolates smooth muscle from various levels of the vascular tree. Isolated aortic and coronary smooth muscle contracts in response to these prostaglandins, but smooth muscle of small arteries (200-1,000 [mu] o.d.) from other sites shows a biphasic dose-response relationship with these compounds. Helical strips from small renal, muscular, and mesenteric arteries, partially contracted by catecholamines, plasma contracting factor, or KC1 are relaxed by prostaglandins in low concentrations and contracted further by prostaglandins in high concentrations. These effects are not abolished by alpha and beta adrenergic blockade, atropine, LSD-25 [lysergic acid diethylamide], or antihista-mine. Prostaglandins mimic the effect of decreased Ca++ concentrations on the rate of rhythmic contraction of isolated rat portal vein and dog ureter strips. The interrelationship of prostaglandins with Ca++ is discussed. The relaxation of isolated smooth muscle from small arteries affords an in vitro model for the study of the vasodepressor action of the prostaglandins.