| pubmed-article:2837460 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2837460 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:2837460 | lifeskim:mentions | umls-concept:C0014563 | lld:lifeskim |
| pubmed-article:2837460 | lifeskim:mentions | umls-concept:C0001455 | lld:lifeskim |
| pubmed-article:2837460 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:2837460 | lifeskim:mentions | umls-concept:C1256369 | lld:lifeskim |
| pubmed-article:2837460 | lifeskim:mentions | umls-concept:C2250323 | lld:lifeskim |
| pubmed-article:2837460 | lifeskim:mentions | umls-concept:C1707520 | lld:lifeskim |
| pubmed-article:2837460 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:2837460 | pubmed:dateCreated | 1988-7-27 | lld:pubmed |
| pubmed-article:2837460 | pubmed:abstractText | The mechanism by which alpha 2-adrenergic agonists inhibit exocytosis was investigated in electrically permeabilized insulin secreting RINm5F cells. In this preparation alpha 2-adrenoceptors remain coupled to adenylate cyclase, since basal- and forskolin-stimulated cyclic AMP production was lowered by epinephrine and clonidine by 30-50%. Cyclic AMP levels did not correlate with the rate of insulin secretion. Thus, at low Ca2+, forskolin enhanced cyclic AMP levels 5-fold without eliciting secretion, and Ca2+-stimulated secretion was associated with decreased cyclic AMP accumulation. Epinephrine (plus propranolol) inhibited Ca2+-induced insulin secretion in a GTP-dependent manner. The maximal inhibition (43%) occurred at 500 microM GTP. Clonidine also inhibited Ca2+-stimulated secretion. Replacement of GTP by GDP or by the nonhydrolyzable GTP analog guanosine 5'-(3-O-thio)triphosphate as well as treatment of the cells with pertussis toxin prior to permeabilization abolished epinephrine inhibition of insulin secretion. Pertussis toxin did not affect Ca2+-stimulated secretion. Insulin release stimulated by 1,2-didecanoyl glycerol was also lowered by epinephrine suggesting an effect distal to the activation of protein kinase C (Ca2+/phospholipid-dependent enzyme). These results taken together with the ability of epinephrine to inhibit ionomycin-induced insulin secretion in intact cells suggest that alpha 2-adrenergic inhibition is distal to the generation of second messengers. A model is proposed for alpha 2-adrenoceptor coupling to two effector systems, namely the adenylate cyclase and the exocytotic site in insulin-secreting cells. | lld:pubmed |
| pubmed-article:2837460 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:2837460 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2837460 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2837460 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:2837460 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:2837460 | pubmed:author | pubmed-author:WollheimC BCB | lld:pubmed |
| pubmed-article:2837460 | pubmed:author | pubmed-author:UllrichSS | lld:pubmed |
| pubmed-article:2837460 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2837460 | pubmed:day | 25 | lld:pubmed |
| pubmed-article:2837460 | pubmed:volume | 263 | lld:pubmed |
| pubmed-article:2837460 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2837460 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2837460 | pubmed:pagination | 8615-20 | lld:pubmed |
| pubmed-article:2837460 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:2837460 | pubmed:year | 1988 | lld:pubmed |
| pubmed-article:2837460 | pubmed:articleTitle | GTP-dependent inhibition of insulin secretion by epinephrine in permeabilized RINm5F cells. Lack of correlation between insulin secretion and cyclic AMP levels. | lld:pubmed |
| pubmed-article:2837460 | pubmed:affiliation | Institut de Biochimie Clinique, Centre Médical Universitaire, Genève, Switzerland. | lld:pubmed |
| pubmed-article:2837460 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2837460 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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