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  • Title: Somatostatin-induced contraction mediated by endothelial TXA2 production in canine cerebral arteries.
    Author: Shirahase H, Kanda M, Shimaji H, Usui H, Rorstad OP, Kurahashi K.
    Journal: Life Sci; 1993; 53(20):1539-44. PubMed ID: 8105357.
    Abstract:
    Whether somatostatin causes endothelium-dependent contraction (EDC) in isolated canine basilar arteries was examined. Somatostatin (10(-8)-10(-6) M) caused transient contractions in a dose-dependent manner. These contractions were abolished by removal of the endothelium, while the contractile response to neuropeptide Y occurred even after removal of the endothelium. The EDC induced by somatostatin (10(-7) M) was affected by neither atropine (10(-6) M) nor cyclo-somatostatin (10(-5) M), which suggests that the EDC is not due to release of endogenous acetylcholine and that the endothelial somatostatin receptor is different from hormonal somatostatin receptors. The somatostatin-induced EDC was attenuated by cyclooxygenase inhibitors (aspirin and indomethacin), thromboxane A2 (TXA2) synthetase inhibitors (OKY-064 and RS-5186), and TXA2 antagonists (ONO-3708 and S-145), which suggests that the endothelium-derived contracting factor is TXA2. These findings demonstrate that somatostatin causes EDC via activation of TXA2 synthesis in canine cerebral arteries.
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