Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1992-12-23
pubmed:abstractText
The presence of the endothelium reduced the sensitivity of isolated rabbit carotid artery to endogenous norepinephrine released by electrical stimulation of adrenergic nerves or displaced by tyramine and to exogenously applied norepinephrine, phenylephrine and UK 14304. The maximal contractions induced by the selective alpha 2-agonist UK 14304 were much more profoundly depressed in arteries with endothelium than those induced by the nonselective alpha-adrenoceptor agonist norepinephrine or by the selective alpha 1-agonist. LY 83583, a cyclic-guanosine-monophosphate (GMP)-lowering agent, abolished the endothelium-dependent depression of tone induced by the agonists and converted the sensitivity of arteries with endothelium to that of endothelium-denuded preparations. M & B 22948, a selective cyclic GMP phosphodiesterase inhibitor, significantly inhibited contractions caused by electrical stimulation of adrenergic nerves, tyramine, norepinephrine and UK 14304 in rings with, but not in those without, endothelium. Yohimbine, an alpha 2-adrenoceptor antagonist, increased contractions caused by UK 14304 in rings with endothelium only, but had no significant effect on the contractions caused by exogenously applied norepinephrine or phenylephrine. In the presence of prazosin, an alpha 1-blocker, UK 14304 caused minimal relaxation (about 20%) in rings with endothelium only which were inhibited by yohimbine, suggesting a minor role of direct endothelial cell alpha 2-mediated release of relaxing factors. The over-flow of endogenous norepinephrine caused by electrical stimulation was not affected by treatment with LY 83583 or M & B 22948, suggesting that altering cyclic GMP levels has no major role in prejunctional modulation of norepinephrine release. These findings support the notion that intrinsic levels of cyclic GMP may act as a regulator of adrenergic neurotransmission due primarily to endothelium-derived relaxing factor which is released basally, and to a lesser extent by an activation of endothelial cell alpha 2-adrenoceptors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1018-1172
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
396-404
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:1358232-Adrenergic alpha-Agonists, pubmed-meshheading:1358232-Aminoquinolines, pubmed-meshheading:1358232-Animals, pubmed-meshheading:1358232-Carotid Arteries, pubmed-meshheading:1358232-Cyclic GMP, pubmed-meshheading:1358232-Dose-Response Relationship, Drug, pubmed-meshheading:1358232-Electric Stimulation, pubmed-meshheading:1358232-Endothelium, Vascular, pubmed-meshheading:1358232-Mice, pubmed-meshheading:1358232-Muscle, Smooth, Vascular, pubmed-meshheading:1358232-Muscle Relaxation, pubmed-meshheading:1358232-Norepinephrine, pubmed-meshheading:1358232-Phenylephrine, pubmed-meshheading:1358232-Purinones, pubmed-meshheading:1358232-Quinoxalines, pubmed-meshheading:1358232-Rabbits, pubmed-meshheading:1358232-Sympathetic Nervous System, pubmed-meshheading:1358232-Synaptic Transmission, pubmed-meshheading:1358232-Tyramine, pubmed-meshheading:1358232-Vasoconstriction
pubmed:articleTitle
Cyclic GMP modulators on vascular adrenergic neurotransmission.
pubmed:affiliation
Robert Dawson Evans Memorial Department of Clinical Research, Boston University School of Medicine, Mass.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't