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, PGE
1 and PGE
2 (10
-9-10
-6g/ml) had no effect on mechanical properties, but PGF
2α (10
-8g/ml) produced tonic contraction, while in the portal vein, PGE
1 and PGE
2 caused relaxation of the tissues. When the tissue of the pulmonary artery contracted from pretreatment with noradrenaline (10
-7g/ml), PGE
1 and PGE
2 experienced partial, incomplete, relaxation, while PGF
2α enhanced the mechanical response produced by noradrenaline.
At concentrations of 10
-7g/ml, PGE
1 and PGE
2 hyperpolarized the membranes in both smooth muscle tissues while PGF
2α depolarized them. These agents decreased membrane resistance at all membrane potential levels to values below those measured in Krebs solution. PGF
2α (10
-6 g/ml) applied simultaneously with procaine (1.4-2.7×10
-3g/ml) markedly enhanced the mechanical responses of both tissues beyond the effects evoked by PGF
2α alone. However, noradrenaline (10
-8 and 10
-7g/ml) applied simultaneously with procaine (1.4×10
-3g/ml) markedly suppressed the mechanical responses evoked by noradrenaline alone.
It is concluded that PGE
1 and PGE
2 brought about relaxation of both tissues (vasodilation). while PGF
2α brought about contraction (vasoconstriction). The excitatory action of PGF
2α (10
-5g/ml) and noradrenaline (10
-7g/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.
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