pubmed-article:9038944 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9038944 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:9038944 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:9038944 | lifeskim:mentions | umls-concept:C0003842 | lld:lifeskim |
pubmed-article:9038944 | lifeskim:mentions | umls-concept:C0039259 | lld:lifeskim |
pubmed-article:9038944 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
pubmed-article:9038944 | lifeskim:mentions | umls-concept:C1167267 | lld:lifeskim |
pubmed-article:9038944 | lifeskim:mentions | umls-concept:C1846431 | lld:lifeskim |
pubmed-article:9038944 | lifeskim:mentions | umls-concept:C1539322 | lld:lifeskim |
pubmed-article:9038944 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
pubmed-article:9038944 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
pubmed-article:9038944 | lifeskim:mentions | umls-concept:C1698986 | lld:lifeskim |
pubmed-article:9038944 | pubmed:issue | 1 Pt 2 | lld:pubmed |
pubmed-article:9038944 | pubmed:dateCreated | 1997-3-31 | lld:pubmed |
pubmed-article:9038944 | pubmed:abstractText | beta-Adrenergic agonists induce the relaxation of vascular smooth muscle by a mechanism that activates the extrusion of Na+ and Ca2+ from the cell. A primary source of contractile Ca2+ resides in the sarcoplasmic reticulum (SR), which releases Ca2+ in response to vasoactive agents through inositol trisphosphate-mediated channels. To determine if smooth muscle relaxation induced by beta 2-adrenergic agonists involves the redistribution of intracellular Ca2+, we studied the effects of isoproterenol (Iso) on freshly isolated, single rat tail artery smooth muscle cells loaded with fura 2, using digital ratiometric fluorescence imaging. Stimulation with 1 microM phenylephrine (PE) or norepinephrine produced phasic and tonic increases in cytoplasmic intracellular Ca2+ concentration ([Ca2+]i) associated associated with cell shortening. Exposure to caffeine and to Ca2(+)-free solutions eliminated the phasic and tonic components, respectively, from the Ca2+ signal. Intermittent superfusion with PE or caffeine was used to evaluate SR Ca2+ stores after stimulation by Iso. Exposure to 1 microM Iso induced a time-dependent decrease in PE-activated peak and tonic [Ca2+]i without any change in resting [Ca2+]i. Intermittent stimulation with 10 mM caffeine revealed a similar decline in peak [Ca2+]i, indicating Iso-dependent depletion of SR Ca2+ stores. The Ca2+ that remained in the SR after prolonged exposure to Iso (30% of the pre-Iso level by 80 min at 22 degrees C) failed to elicit a contractile response. The cells, perfused with a Na(+)- and Ca2(+)-free medium to block Na+/ Ca2+ exchange, prevented depletion of the SR Ca2+ stores by Iso. We propose that Iso inhibits agonist-mediated Ca2+ influx through sarcolemmal Ca2+ channels and activates Ca2+ redistribution from storage sites in the SR to the extracellular compartment by a mechanism that involves Na+/Ca2+ exchange. These combined effects of Iso facilitate smooth muscle relaxation (and reduce vascular tonus) by reducing the increase in cytoplasmic Ca2+ evoked by vasoconstrictors. | lld:pubmed |
pubmed-article:9038944 | pubmed:language | eng | lld:pubmed |
pubmed-article:9038944 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9038944 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9038944 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9038944 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9038944 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9038944 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9038944 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9038944 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9038944 | pubmed:month | Jan | lld:pubmed |
pubmed-article:9038944 | pubmed:issn | 0002-9513 | lld:pubmed |
pubmed-article:9038944 | pubmed:author | pubmed-author:ChengLL | lld:pubmed |
pubmed-article:9038944 | pubmed:author | pubmed-author:MiyashitaYY | lld:pubmed |
pubmed-article:9038944 | pubmed:author | pubmed-author:KonKK | lld:pubmed |
pubmed-article:9038944 | pubmed:author | pubmed-author:LakattaE GEG | lld:pubmed |
pubmed-article:9038944 | pubmed:author | pubmed-author:FroehlichJ... | lld:pubmed |
pubmed-article:9038944 | pubmed:author | pubmed-author:KinsellaJ LJL | lld:pubmed |
pubmed-article:9038944 | pubmed:author | pubmed-author:SollottS JSJ | lld:pubmed |
pubmed-article:9038944 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9038944 | pubmed:volume | 272 | lld:pubmed |
pubmed-article:9038944 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9038944 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9038944 | pubmed:pagination | H244-55 | lld:pubmed |
pubmed-article:9038944 | pubmed:dateRevised | 2003-11-14 | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:meshHeading | pubmed-meshheading:9038944-... | lld:pubmed |
pubmed-article:9038944 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9038944 | pubmed:articleTitle | Redistribution of intracellular Ca2+ stores after beta-adrenergic stimulation of rat tail artery SMC. | lld:pubmed |
pubmed-article:9038944 | pubmed:affiliation | Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA. | lld:pubmed |
pubmed-article:9038944 | pubmed:publicationType | Journal Article | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9038944 | lld:pubmed |