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,), PGA 2 , PGB 1 , PGD 2 , PGE, 1 , PGE 2 or to PGF lα . However, high concentrations of both PGB 2 (> 10 −7 m) and PGF 2α (> 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 contrtactions. 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 2α > PGA 2 »PGA 1 , > PGF 1α > 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 × 10 −8 to 3.4 × 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.