Prostaglandin action on the main pulmonary artery and portal vein of the rabbit.

The effects of prostaglandins on electrical and mechanical properties of the rabbit pulmonary artery and portal vein were investigated and compared with those recorded from the guinea pig. In the pulmonary artery, PGE1 and PGE2 (10(-9)-10(-6) g/ml) had no effect on mechanical properties, but PGF2alpha (10(-8) g/ml) produced tonic contraction, while in the portal vein, PGE1 and PGE2 caused relaxation of the tissues. When the tissue of the pulmonary artery contracted from pretreatment with noradrenaline (10(-7) g/ml), PGE1 and PGE2 experienced partial, incomplete, relaxation, while PGF2alpha enhanced the mechanical response produced by noradrenaline. At concentrations of 10(-7) g/ml, PGE1 and PGE2 hyperpolarized the membranes in both smooth muscle tissues while PGF2alpha depolarized them. These agents decreased membrane resistance at all membrane potential levels to values below those measured in Krebs solution. PGF2alpha (10(-6) g/ml) applied simultaneously with procaine (1.4-2.7 x 10(-3) g/ml) markedly enhanced the mechanical responses of both tissues beyond the effects evoked by PGF2alpha alone. However, noradrenaline (10(-8) and 10(-7) g/ml) applied simultaneously with procaine (1.4 x 10(-3) g/ml) markedly suppressed the mechanical responses evoked by noradrenaline alone. It is concluded that PGE1 and PGE2 brought about relaxation of both tissues (vasodilation), while PGF2alpha brought about contraction (vasoconstriction). The excitatory action of PGF2alpha (10(-5) g/ml) and noradrenaline (10(-7) g/ml) on the electrical and mechanical responses appear as the same phenomena, i.e., depolarized membrane, decreased membrane resistance and contraction, although the mechanisms producing the above phenomena differ.