Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1984-9-17
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
230
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
413-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1984
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.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't