Inhibition of Untransformed Prostaglandin H2 Production and Stretch-Induced Contraction of Rabbit Pulmonary Arteries by Indoxam, a Selective Secretory Phospholipase A2 Inhibitor

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  • Tanabe Yoshiyuki
    Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University, Japan Department of Cellular and Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka, Japan
  • Saito Maki
    Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University, Japan
  • Morikawa Yuki
    Department of Cellular and Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka, Japan
  • Kamataki Akihisa
    Department of Pathology, School of Medicine, Iwate Medical University, Japan
  • Sawai Takashi
    Department of Pathology, School of Medicine, Iwate Medical University, Japan
  • Hirose Masamichi
    Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University, Japan
  • Nakayama Koichi
    Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University, Japan Department of Cellular and Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka, Japan

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Involvement of secretory phospholipase A2 (sPLA2) in the stretch-induced production of untransformed prostaglandin H2 (PGH2) in the endothelium of rabbit pulmonary arteries was investigated. The stretch-induced contraction was significantly inhibited by indoxam, a selective inhibitor for sPLA2, and NS-398, a selective inhibitor for cyclooxygenase-2 (COX-2). Indoxam inhibited the RGD-sensitive-integrin–independent production of untransformed PGH2, but did not affect the RGD-sensitive-integrin–dependent production of thromboxane A2 (TXA2). These results suggest that the stretch-induced contraction and untransformed PGH2 production was mediated by sPLA2–COX-2 pathway, making it a new possible target for pharmacological intervention of pulmonary artery contractility.

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