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Vol. 299, Issue 2, 768-774, November 2001

Colitis-Induced Alterations in Adrenergic Control of Circular Smooth Muscle in Vitro in Rats

Aiping Zhao, Carol Bossone, Victor Piñeiro-Carrero and Terez Shea-Donohue

Departments of Medicine (A.Z., T.S.-D.) and Pediatrics (V.P.-C.), Uniformed Services University of the Health Sciences, Bethesda, Maryland; and Walter Reed Army Institute of Research, Forest Glen, Maryland (C.B.)

The present study investigated inflammation-induced changes in adrenergic regulation of smooth muscle. Colitis was induced in rats by intrarectal administration of trinitrobenzenesulfonic acid in ethanol. After 4 h (acute) or 7 days (chronic), in vitro isometric tension was measured in strips of circular smooth muscle taken from the distal colon. In controls, the major inhibitory control of smooth muscle responses to nerve stimulation was mediated by nitric oxide and beta  adrenergic receptors. There was less evidence of alpha  adrenergic control. Studies with the beta 3 receptor antagonist cyanopindolol and the beta 3 receptor agonist BRL37344 revealed that beta  adrenergic regulation of spontaneous contractions and responses to nerve stimulation were mediated primarily by the beta 3 adrenoreceptor. Both acute and chronic colitis significantly increased responses to electrical field stimulation. This effect was attributed to a loss of inhibitory nitrergic regulation as well as to selective changes in the beta  adrenergic control of colonic circular smooth muscle. Inflammation did not alter alpha  adrenergic control. Chronic colitis also decreased the sensitivity to nerve stimulation and pharmacological contractile agents. Acute and chronic inflammation reduced the ability of BRL37344 to inhibit contractions in response to nerve stimulation. In addition, in inflamed colon, BRL37344 was less effective in relaxing carbachol-induced precontractions. Finally, inflammation resulted in a loss of the ability of the cyanopindolol to increase the amplitude of both spontaneous contractions and contractions in response to nerve stimulation. These effects indicated that colitis induced a down-regulation of inhibitory beta 3 adrenergic control of colonic smooth muscle function. This loss of adrenergic regulation may contribute to the diarrhea in inflammatory bowel disease.

0022-3565/01/2992-0768$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 2001 by U.S. Government


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