{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,17]],"date-time":"2023-10-17T01:12:14Z","timestamp":1697505134503},"reference-count":49,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2001,12,7]],"date-time":"2001-12-07T00:00:00Z","timestamp":1007683200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2002,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We studied the effects of increased Ca<jats:sup>2+<\/jats:sup> influx on \u03b1<jats:sub>1<\/jats:sub>\u2010adrenoceptor\u2010stimulated InsP formation in adult rat cardiac myocytes. We further examined if such effects could be mediated through a specific \u03b1<jats:sub>1<\/jats:sub>\u2010adrenoceptor subtype. [<jats:sup>3<\/jats:sup>H]InsP responses to adrenaline were dependent on extracellular Ca<jats:sup>2+<\/jats:sup> concentration, from 0.1 \u03bcM to 2 mM, and were completely blocked by Ca<jats:sup>2+<\/jats:sup> removal. However, in cardiac myocytes preloaded with BAPTA, a highly selective calcium chelating agent, Ca<jats:sup>2+<\/jats:sup> concentrations higher than 1 \u03bcM had no effect on adrenaline\u2010stimulated [<jats:sup>3<\/jats:sup>H]InsP formation. Taken together these results suggest that [<jats:sup>3<\/jats:sup>H]InsP formation induced by \u03b1<jats:sub>1<\/jats:sub>\u2010adrenergic stimulation is in part mediated by increased Ca<jats:sup>2+<\/jats:sup> influx. Consistent with this, ionomycin, a calcium ionophore, stimulated [<jats:sup>3<\/jats:sup>H]InsP formation. This response was additive with the response to adrenaline stimulation implying that different signaling mechanisms may be involved. In cardiac myocytes treated with the \u03b1<jats:sub>1B<\/jats:sub>\u2010adrenoceptor alkylating agent, CEC, [<jats:sup>3<\/jats:sup>H]InsP formation remained unaffected by increased Ca<jats:sup>2+<\/jats:sup> concentrations, a pattern similar to that observed when intracellular Ca<jats:sup>2+<\/jats:sup> was chelated with BAPTA. In contrast, addition of the \u03b1<jats:sub>1A<\/jats:sub>\u2010subtype antagonist, 5\u2032\u2010methyl urapidil, did not affect the Ca<jats:sup>2+<\/jats:sup> dependence of [<jats:sup>3<\/jats:sup>H]InsP formation. Neither nifedipine, a voltage\u2010dependent Ca<jats:sup>2+<\/jats:sup> channel blocker nor the inorganic Ca<jats:sup>2+<\/jats:sup> channel blockers, Ni<jats:sup>2+<\/jats:sup> and Co<jats:sup>2+<\/jats:sup>, had any effect on adrenaline stimulated [<jats:sup>3<\/jats:sup>H]InsP, at concentrations that inhibit Ca<jats:sup>2+<\/jats:sup> channels. The results suggest that in adult rat cardiac myocytes, in addition to G protein\u2010mediated response, \u03b1<jats:sub>1<\/jats:sub>\u2010adrenergic\u2010stimulated [<jats:sup>3<\/jats:sup>H]InsP formation is activated by increased Ca<jats:sup>2+<\/jats:sup> influx mediated by the \u03b1<jats:sub>1B<\/jats:sub>\u2010subtype. J. Cell. Biochem. 84: 201\u2013210, 2002. \u00a9 2001 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcb.1281","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T21:17:12Z","timestamp":1030310232000},"page":"201-210","source":"Crossref","is-referenced-by-count":0,"title":["\u03b1<sub>1<\/sub>\u2010adrenergic stimulation mediates Ca<sup>2+<\/sup>\u2010dependent inositol phosphate formation through the \u03b1<sub>1B<\/sub>\u2010like adrenoceptor subtype in adult rat cardiac 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