The Role of Nitric Oxide in the Electrical Field Stimulation-Induced Contractions of Sphincter of Oddi and Gallbladder Strips in Guinea Pigs

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  • Gultekin Hulya
    Department of Pharmacology, Faculty of Medicine, Erciyes University, Turkey
  • Erdem S. Remzi
    Department of Pharmacology, Faculty of Medicine, Baskent University, Turkey
  • Emre-Aydingoz Selda
    1703 Bluejay Cove, St. Louis, MO 63144, USA
  • Tuncer Meral
    Department of Pharmacology, Faculty of Medicine, Hacettepe University, Turkey

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  • Role of Nitric Oxide in the Electrical Field Stimulation Induced Contractions of Sphincter of Oddi and Gallbladder Strips in Guinea Pigs

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Abstract

The aim of this study was to investigate the modulatory role of nitric oxide (NO) in the electrical field stimulation (EFS)-induced contractions of isolated sphincter of Oddi (SO) and gallbladder strips from guinea pigs. EFS was used to activate the intrinsic nerves in SO and gallbladder strips. EFS produced frequency-dependent biphasic contractile responses in the SO strips. A smaller contraction, “on response”, occurred during EFS, which was followed by a bigger contraction, “off response”. Both responses were completely and irreversibly abolished by tetrodotoxin (TTX) (10−6 M). Atropine (10−6 M) inhibited the “on response”, but not the “off response”. EFS produced frequency-dependent monophasic contractile responses in gallbladder strips, which were completely and irreversibly abolished by TTX (10−6 M) and atropine (10−6 M). A nitric oxide synthase (NOS) inhibitor, NG-nitro-<sc>L</sc>-arginine (10−4 M and 3 × 10−4 M, in SO and gallbladder strips, respectively), significantly increased all EFS-induced contractions of SO and gallbladder strips. <sc>L</sc>-Arginine, but not <sc>D</sc>-arginine reversed the effect induced by the NOS inhibitor, at all frequencies, in both strips. These results suggested that NO released from nitrergic nerve endings might play a regulatory role in the cholinergic neurotransmission of guinea pig SO and gallbladder strips. The “off response” in he SO preparations might be a rebound increase that was modulated by the nonadrenergic, noncholinergic inhibitory mediator NO.<br>

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