Add time:08/03/2019         Source:sciencedirect.com

1.1. In isolated rat aortic rings, leminoprazole (2-[2-N-methyl-N-(2-methylpropyl)amino] benzylsulfinyl benzimidazole) (10−6-10−4 M) inhibited contractile responses to phenylephrine (PE), KCl and Ca2+ in KCl-depolarized tissues in a Ca2+ free medium. Leminoprazole also relaxed the aorta contracted by PE and KCI.2.2. The relaxing effect of leminoprazole was markedly inhibited by nifedipine and verapamil (inhibitors of voltage operated Ca2+ channels). Relaxation induced by verapamil, but not by nifedipine, was inhibited by pre-treatment by leminoprazole.3.3. The relaxing effect of leminoprazole was also inhibited by NG-monomethyl-l-arginine (a nitric oxide synthase inhibitor), methylene blue (a guanylate cyclase inhibitor) or endothelium removal but not by indomethacin (a cyclooxygenase inhibitor), glyburide (a KATP channel inhibitor) or iberiotoxin (a KCa channel inhibitor).4.4. Zaprinast (a cGMP-phosphodiesterase inhibitor) also inhibited the relaxing action of leminoprazole. In addition, relaxation induced by nitroglycerin was potentiated by leminoprazole.5.5. Further, in the presence of methylene blue, residual relaxation induced by leminoprazole was still potentiated by verapamil.6.6. These results suggest that the vasoinhibitory effect of leminoprazole in rat aortic rings is due to the increased level of cGMP through inhibition of cGMP-phosphodiesterase and also due to inhibition of voltage operated Ca2+ channels.

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