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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0005847,
umls-concept:C0025474,
umls-concept:C0028351,
umls-concept:C0030685,
umls-concept:C0178719,
umls-concept:C0205263,
umls-concept:C0205409,
umls-concept:C0391871,
umls-concept:C0596235,
umls-concept:C0597357,
umls-concept:C0680255,
umls-concept:C0683598,
umls-concept:C1283071,
umls-concept:C1879547,
umls-concept:C1882561,
umls-concept:C1963578,
umls-concept:C1979844
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pubmed:issue |
2
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pubmed:dateCreated |
1984-9-17
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pubmed:abstractText |
This study was undertaken to determine which alpha adrenoceptor subtype(s) is involved in the activation of isolated rat aorta and mesenteric resistance vessels by norepinephrine and to ascertain whether norepinephrine-induced Ca++ influx into the smooth muscle is activated by one alpha adrenoceptor subtype while intracellular Ca++ release is mediated by the other subtype. The concentration-response curves for prazosin and yohimbine inhibition of norepinephrine-induced 45Ca influx, intracellular Ca++ release (as judged from contractions in Ca++-free solution) and contraction in the rat aorta indicate that the norepinephrine activation of the alpha-1 adrenoceptor was responsible for both Ca++ mobilization processes leading to norepinephrine contraction of this tissue. Contractions induced by norepinephrine in the isolated rat mesenteric resistance vessels demonstrated a phasic component, which was shown to be primarily dependent on intracellular Ca++ release, and a tonic component, which was completely dependent on Ca++ influx. Prazosin was three orders of magnitude more potent than yohimbine in inhibiting both components of the norepinephrine contracture in these vessels. We conclude that norepinephrine activation of alpha-1 adrenoceptors is responsible for both Ca++ influx and intracellular Ca++ release in isolated rat aorta and mesenteric resistance vessels.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Prazosin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Yohimbine
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0022-3565
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
230
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
413-8
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:6086886-Animals,
pubmed-meshheading:6086886-Aorta,
pubmed-meshheading:6086886-Calcium,
pubmed-meshheading:6086886-Mesenteric Arteries,
pubmed-meshheading:6086886-Mesenteric Veins,
pubmed-meshheading:6086886-Muscle, Smooth, Vascular,
pubmed-meshheading:6086886-Muscle Contraction,
pubmed-meshheading:6086886-Norepinephrine,
pubmed-meshheading:6086886-Prazosin,
pubmed-meshheading:6086886-Rats,
pubmed-meshheading:6086886-Rats, Inbred Strains,
pubmed-meshheading:6086886-Receptors, Adrenergic, alpha,
pubmed-meshheading:6086886-Vasoconstriction,
pubmed-meshheading:6086886-Yohimbine
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pubmed:year |
1984
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pubmed:articleTitle |
Induction of Ca++ influx and intracellular Ca++ release in isolated rat aorta and mesenteric resistance vessels by norepinephrine activation of alpha-1 receptors.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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