Abstract.
The possible involvement of the endocardial endothelium in the positive inotropic response of the mouse left atrium to acetylcholine was examined pharmacologically. In mouse left atria, acetylcholine produced a biphasic inotropic response: a transient decrease in contractile force followed by a late increase. The positive response was not affected by the presence of phentolamine and propranolol, but was almost abolished by pretreatment of the preparation with 1% Triton X-100, which denudes the endocardium of its endothelium. Nordihydroguaiaretic acid, N G-nitro-L-arginine, BQ-123 and BQ-788 had no effect on the inotropic responses to acetylcholine, but indomethacin completely abolished the positive response. Prostaglandins and their analogues had a positive inotropic effect with a potency order PGF2 α>PGD2>PGE2>U46619, whereas beraprost had no effect. Neither Triton X-100 pretreatment nor the presence of indomethacin affected the positive inotropic effect of PGF2 α. Acetylcholine and PGF2 α prolonged the action potential duration similarly. These results suggest that the acetylcholine-induced positive inotropic response in mouse left atria is mediated by prostaglandin released from the endocardial endothelium.
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Tanaka, H., Nishimaru, K., Kobayashi, M. et al. Acetylcholine-induced positive inotropy mediated by prostaglandin released from endocardial endothelium in mouse left atrium. Naunyn-Schmied Arch Pharmacol 363, 577–582 (2001). https://doi.org/10.1007/s002100100411
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DOI: https://doi.org/10.1007/s002100100411