Linked Life Data

11457599

Source:http://linkedlifedata.com/resource/pubmed/id/11457599

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-7-17
pubmed:abstractText
Nitric oxide has various actions, acting in a neurotransmitter-like role and also as a paracrine messenger between vascular endothelial and smooth muscle cells. This study was done to determine whether endogenous nitric oxide has a role in modulating evoked catecholamine release from the canine adrenal medulla. Isolated adrenal glands were perfused with Krebs-Ringer solution as a control, or with Krebs-Ringer solution containing either N(G)-monomethyl-L-arginine (L-NMMA; 3x10(-4) M) to non-selectively inhibit nitric oxide synthase or 7-nitroindazole (10(-4) M), a relatively selective inhibitor of neuronal nitric oxide synthase. Catecholamine release was evoked using the nicotinic cholinergic agonist 1,1-dimethyl-4-phenylpiperazinium iodine. From the collected perfusate epinephrine, norepinephrine, and dopamine were measured by high performance liquid chromatography. Previous studies have shown that in the presence of L-NMMA, basal releases of epinephrine, norepinephrine and dopamine are increased. 7-Nitroindazole had no effect on basal catecholamine release, suggesting that nitric oxide from an endothelial source was responsible for the inhibition of basal catecholamine release from the adrenal medulla. Epinephrine and norepinephrine releases were augmented when either of the nitric oxide synthase inhibitors was added during submaximal nicotinic stimulation, indicating that endogenous nitric oxide inhibited release of epinephrine and norepinephrine. Both neuronal and endothelial nitric oxide synthases appeared to be responsible for this inhibition. In summary, these studies suggest that nitric oxide, from both neuronal and endothelial sources, modulates evoked catecholamine release from canine adrenal medulla, while nitric oxide from an endothelial source is most likely responsible for modulation of catecholamine release under basal conditions.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
104
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1165-73
pubmed:dateRevised
2009-11-3
pubmed:meshHeading
pubmed-meshheading:11457599-Adrenal Medulla, pubmed-meshheading:11457599-Animals, pubmed-meshheading:11457599-Catecholamines, pubmed-meshheading:11457599-Chromaffin Cells, pubmed-meshheading:11457599-Dimethylphenylpiperazinium Iodide, pubmed-meshheading:11457599-Dogs, pubmed-meshheading:11457599-Dopamine, pubmed-meshheading:11457599-Dose-Response Relationship, Drug, pubmed-meshheading:11457599-Enzyme Inhibitors, pubmed-meshheading:11457599-Epinephrine, pubmed-meshheading:11457599-Female, pubmed-meshheading:11457599-Indazoles, pubmed-meshheading:11457599-Male, pubmed-meshheading:11457599-Nicotinic Agonists, pubmed-meshheading:11457599-Nitric Oxide, pubmed-meshheading:11457599-Nitric Oxide Synthase, pubmed-meshheading:11457599-Norepinephrine, pubmed-meshheading:11457599-omega-N-Methylarginine
pubmed:year
2001
pubmed:articleTitle
Nitric oxide modulates evoked catecholamine release from canine adrenal medulla.
pubmed:affiliation
Department of Anesthesiology, Mayo Clinic/Foundation, 200 First Street SW, Rochester, MN 55905, USA. barnes.roxann@mayo.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't