pubmed-article:3228676 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:3228676 | lifeskim:mentions | umls-concept:C0035983 | lld:lifeskim |
pubmed-article:3228676 | lifeskim:mentions | umls-concept:C0005847 | lld:lifeskim |
pubmed-article:3228676 | lifeskim:mentions | umls-concept:C0025474 | lld:lifeskim |
pubmed-article:3228676 | lifeskim:mentions | umls-concept:C1882561 | lld:lifeskim |
pubmed-article:3228676 | lifeskim:mentions | umls-concept:C0233494 | lld:lifeskim |
pubmed-article:3228676 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:3228676 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
pubmed-article:3228676 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
pubmed-article:3228676 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:3228676 | pubmed:dateCreated | 1989-4-13 | lld:pubmed |
pubmed-article:3228676 | pubmed:abstractText | 1. The effect of ryanodine on contractile responses dependent either on intracellular Ca2+ release or on extracellular Ca2+ influx were studied in aorta and mesenteric resistance vessels of the rat. 2. In aorta, in the presence of extracellular Ca2+, pretreatment with ryanodine (10(-5)M) did not modify contractile responses to noradrenaline (NA) (10(-6)M) whereas in the absence of Ca2+, pretreatment with ryanodine reduced to about 25% the contractile response to NA (10(-6)M) and totally abolished the transient contraction elicited by caffeine (5 x 10(-2)M). 3. In mesenteric resistance vessels, ryanodine (10(-5)M) had no effects on NA (10(-5)M)-induced tension in the presence of extracellular Ca2+ but totally abolished contractile responses to caffeine (10(-2)M) in the absence of Ca2+. 4. In K+ -depolarized mesenteric resistance vessels, pretreatment with ryanodine (10(-5)M) significantly enhanced contractile responses to Ca2+ concentrations higher than 10(-4)M and 10(-3)M for arteries depolarized with 30 mM and 40 mM K+ respectively. Concentrations of either diltiazem (6 x 10(-7)M) or nifedipine (10(-8)M) that abolished contractile responses to Ca2+ in depolarized arteries (K+, 40 mM) did not totally inhibit the enhancement of Ca2+ -induced contractions obtained in the presence of ryanodine. 5. Ryanodine did not modify the Ca2+ concentration-effect relationships in mesenteric resistance vessels exposed to NA or arginine vasopressin. 6. These data are consistent with the hypothesis that ryanodine induces a release of Ca2+ from intracellular stores, resulting in a subsequent reduction of the amplitude of contractions dependent upon intracellular Ca2+ liberation. Furthermore, the ability of sarcoplasmic reticulum to buffer rises in cytoplasmic Ca2+ may be reduced in the presence of ryanodine, thereby accounting for the potentiation of contractile responses to Ca2+ in K+-depolarized mesenteric resistance vessels. | lld:pubmed |
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pubmed-article:3228676 | pubmed:language | eng | lld:pubmed |
pubmed-article:3228676 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:3228676 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:3228676 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:3228676 | pubmed:month | Oct | lld:pubmed |
pubmed-article:3228676 | pubmed:issn | 0007-1188 | lld:pubmed |
pubmed-article:3228676 | pubmed:author | pubmed-author:FreslonJ LJL | lld:pubmed |
pubmed-article:3228676 | pubmed:author | pubmed-author:Julou-Schaeff... | lld:pubmed |
pubmed-article:3228676 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:3228676 | pubmed:volume | 95 | lld:pubmed |
pubmed-article:3228676 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:3228676 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:3228676 | pubmed:pagination | 605-13 | lld:pubmed |
pubmed-article:3228676 | pubmed:dateRevised | 2010-9-10 | lld:pubmed |
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pubmed-article:3228676 | pubmed:meshHeading | pubmed-meshheading:3228676-... | lld:pubmed |
pubmed-article:3228676 | pubmed:year | 1988 | lld:pubmed |
pubmed-article:3228676 | pubmed:articleTitle | Effects of ryanodine on tension development in rat aorta and mesenteric resistance vessels. | lld:pubmed |
pubmed-article:3228676 | pubmed:affiliation | Université Louis Pasteur, UA CNRS 600, Illkirch, France. | lld:pubmed |
pubmed-article:3228676 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:3228676 | pubmed:publicationType | In Vitro | lld:pubmed |
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