Ca2+ channel blockers interact with α2-adrenergic receptors in rabbit ileum

F. R. Homaidan, M. Donowitz, J. Wicks, S. Cusolito, M. E. El Sabban, G. A. Weiland, G. W.G. Sharp

Research output: Contribution to journalArticle

Abstract

An interaction between Ca2+ channel blockers and α2-adrenergic receptors has been demonstrated in rabbit ileum by studying the effect of clonidine on active electrolyte transport, under short-circuited conditions, in the presence and absence of several Ca2+ channel blocking agents. Clonidine, verapamil, diltiazem, cadmium, and nitrendipine all decrease short-circuit current and stimulate NaCl absorption to different extents with clonidine having the largest effect. Exposure to verapamil, diltiazem, and cadmium inhibited the effects of clonidine on transport, whereas nitrendipine had no such effect. Verapamil, diltiazem, and cadmium, but not nitrendipine, also decreased the specific binding of [3H]α2-adrenergic agents to a preparation of ileal basolateral membranes explaining the observed decrease in the transport effects of clonidine. The effective concentrations of the Ca2+ channel blockers that inhibited the effects of clonidine on transport were fairly similar to the concentrations needed to inhibit its specific binding. The displacement of clonidine by calcium channel blockers is ascribed to a nonspecific effect of these agents, although the possibility that their effects are exerted via their binding to the calcium channels is not excluded.

Original languageEnglish (US)
Pages (from-to)G586-G594
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume254
Issue number4 (17/4)
StatePublished - 1988

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)

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    Homaidan, F. R., Donowitz, M., Wicks, J., Cusolito, S., El Sabban, M. E., Weiland, G. A., & Sharp, G. W. G. (1988). Ca2+ channel blockers interact with α2-adrenergic receptors in rabbit ileum. American Journal of Physiology - Gastrointestinal and Liver Physiology, 254(4 (17/4)), G586-G594.