Differential effects of prostaglandins on canine intrapulmonary arteries and veins.

1 The sensitivity and contractility of isolated canine intrapulmonary arteries and veins to a variety of primary prostaglandin compounds was studied.2 Intrapulmonary arteries produced no measurable contractile responses to prostaglandin A(1) (PGA(1)), PGA(2), PGB(1), PGD(2), PGE(1), PGE(2) or to PGF(1alpha). However, high concentrations of both PGB(2) (> 10(-7) M) and PGF(2alpha) (> 10(-6) M) elicited concentrated-related, but weak, contractile responses, measuring only 5-25% of KCl-induced maximum contractions.3 Intrapulmonary arteries, partially contracted by 5-hydroxytryptamine (5-HT), exhibited concentration-related relaxations in response to PGE(1); PGE(2), PGA(1) or PGA(2) produced only weak superimposed contractions.4 In contrast to intrapulmonary arteries, intrapulmonary veins contracted in a concentration-related fashion to all prostaglandins tested, where the contractile sensitivity was (based on EC(50) s and threshold concentrations): PGB(2) > PGB(1) > PGD(2) > PGF(2alpha) > PGA(2) >> PGA(1) > PGF(1alpha) > PGE(2) > PGE(1).5 In terms of the ability to generate maximum contractile responses on intrapulmonary veins, the prostaglandins were also variable, with PGA(2) and PGB(2) being the most potent and PGD(2) the least potent.6 Intrapulmonary veins, partially contracted by 5-HT, exhibited concentration-related relaxations to PGE(1) at low concentrations, followed by secondary contractile responses at higher concentrations.7 Neither PGA(1) nor PGA(2) (3.4 x 10(-8) to 3.4 x 10(-5) M) inhibited or potentiated 5-HT responses of intrapulmonary arteries.8 These data suggest that there are species, regional and major qualitative and quantitative, differences in the responsiveness of intrapulmonary arteries and veins to prostaglandin.