PROSTACYCLIN AND THROMBOXANE-A2 SYNTHESIS BY RABBIT PULMONARY-ARTERY

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  • 1 January 1980
    • journal article
    • research article
    • Vol. 215  (1) , 240-247
Abstract
Superfused spiral strips of rabbit intrapulmonary artery (i.p.a.) were contracted by arachidonic acid (AA) and by the following substances in order of potency: prostaglandin (PG) endoperoxide analog (U46619) > PGH2 > PGF2.alpha.. Intrapulmonary artery strips were consistently relaxed by PGE2 and by the enzyme inhibitors, indomethacin, aspirin, meclofenamic acid and 1-pentylimidazole. The cyclooxygenase and thromboxane (TX) synthetase inhibitors blocked the AA-induced contraction of rabbit i.p.a. Prostacyclin (PGI2) had no effect on the i.p.a. or produced a small contraction or relaxation. TXA2, formed by incubating horse platelet microsomes with PGH2, contracted the tissue and was more potent than the parent endoperoxide. Incubations of [14C]AA with i.p.a. produced [14C]-6-keto-PGF1.alpha. (the breakdown product of PGI2) and [14C]TXB2 (the breakdown product of TXA2); the identities of these products were confirmed by radioimmunoassay and by gas chromatography-mass spectrometry. The synthesis of TXB2 by i.p.a. cannot be attributed to adhering lung tissue or platelets and appears to be produced by the vascular tissue itself. PGI2 and Tx may contribute to the resting tone of the rabbit i.p.a., the response to AA is due to production of TXA2.