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Beta-adrenergic and prostanoid inhibition of canine fundic mucosal mast cells

Beta-adrenergic and prostanoid inhibition of canine fundic mucosal mast cells J. Physiol. 256 (Gastrointest. Liver Physiol. 19): G727-G732, 1989.-We examined regulation canine hepatic and mucosal in short-term culture. We found that ,8-but not a-adrenergicagonistsmarkedly inhibited concanavalin A (ConA) -stimulated . by epinephrine was reversed by the ,&antagonist propranolol, but not by the cr-adrenergicantagonistsphentolamine or yohimbine. The ,&-selective antagonist ICI 115881 reversedthe effects epinephrine, whereasthe &-antagonists practolol and betaxolol had little effect. Prostaglandin ES (PGEZ), but not its analogueenprostil, inhibited ConA-stimulated . This difference may relate to the ability PGEZ, but not enprostil, to stimulate adenosine3’,5’-cyclic monophosphate (CAMP) production. Forskolin, CAMP analogues,and the phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine also effectively inhibited ConA-stimulated .Neither adrenergic agonists nor PGE2 inhibited stimulated by the combination phorbol l2myristate-13-acetateplusthe calcium ionophoreA23187. These data suggest that wasmediatedvia CAMP-dependent mechanisms was exerted on primary cell activation, rather and than on postreceptor activating events. cosal , content appeared to be fully accounted for by the presence , with no evidence supporting the existence in endocrine (1, 26). We have recently reported methods for studying canine enriched by elutriation and placed in short-term culture (27). After overnight suspension culture, were viable and responded to the receptor-mediated stimuli, concanavalin A (ConA) and adenosine, and to agents that activate postreceptor mechanisms, the http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Gastrointestinal and Liver Physiology The American Physiological Society

Beta-adrenergic and prostanoid inhibition of canine fundic mucosal mast cells

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Publisher
The American Physiological Society
Copyright
Copyright © 1989 the American Physiological Society
ISSN
0193-1857
eISSN
1522-1547
Publisher site
See Article on Publisher Site

Abstract

J. Physiol. 256 (Gastrointest. Liver Physiol. 19): G727-G732, 1989.-We examined regulation canine hepatic and mucosal in short-term culture. We found that ,8-but not a-adrenergicagonistsmarkedly inhibited concanavalin A (ConA) -stimulated . by epinephrine was reversed by the ,&antagonist propranolol, but not by the cr-adrenergicantagonistsphentolamine or yohimbine. The ,&-selective antagonist ICI 115881 reversedthe effects epinephrine, whereasthe &-antagonists practolol and betaxolol had little effect. Prostaglandin ES (PGEZ), but not its analogueenprostil, inhibited ConA-stimulated . This difference may relate to the ability PGEZ, but not enprostil, to stimulate adenosine3’,5’-cyclic monophosphate (CAMP) production. Forskolin, CAMP analogues,and the phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine also effectively inhibited ConA-stimulated .Neither adrenergic agonists nor PGE2 inhibited stimulated by the combination phorbol l2myristate-13-acetateplusthe calcium ionophoreA23187. These data suggest that wasmediatedvia CAMP-dependent mechanisms was exerted on primary cell activation, rather and than on postreceptor activating events. cosal , content appeared to be fully accounted for by the presence , with no evidence supporting the existence in endocrine (1, 26). We have recently reported methods for studying canine enriched by elutriation and placed in short-term culture (27). After overnight suspension culture, were viable and responded to the receptor-mediated stimuli, concanavalin A (ConA) and adenosine, and to agents that activate postreceptor mechanisms, the

Journal

AJP - Gastrointestinal and Liver PhysiologyThe American Physiological Society

Published: Apr 1, 1989

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