Linked Life Data

16357097

Source:http://linkedlifedata.com/resource/pubmed/id/16357097

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2006-4-10
pubmed:abstractText
Endothelin (ET) peptides stimulate vasopressin (AVP) secretion via ET(B) receptors at hypothalamic loci. Nitric oxide modulates the actions of ET in the cardiovascular system and also influences neurotransmission and specifically suppresses firing of magnocellular neurons. The purpose of these studies was to ascertain whether nitric oxide, generated in response to ET(B) receptor stimulation, buffers the stimulatory effect of ET and suppresses AVP release. Studies were performed using a pharmacological approach in hypothalamo-neurohypophyseal explants from rats, and an alternative strategy using explants from mice with an inactivating mutation of neuronal NOS (nNOS-/-) and their wild-type parent strain. Whole explants in standard culture or only the hypothalamus of compartmentalized explants was exposed to the ET(B) selective agonist, IRL 1620 (10(-13) to 10(-8) M). Rat and wild-type mouse explants displayed similar responses, although absolute basal release rates were higher from murine explants. Maximal AVP release at 0.1 nM IRL 1620 was 311 +/- 63 (rat) and 422 +/- 112% basal x explant(-1) x h(-1) (mouse). Sodium nitroprusside (SNP; 0.1 mM) suppressed maximal AVP release to basal values. N(omega)-nitro-L-arginine methyl ester (L-NAME, 0.1 microM), which did not itself stimulate AVP secretion, more than doubled the response to 1 pM IRL 1620, from 136 +/- 28 to 295 +/- 49% basal x explant(-1) x h(-1) (P < 0.05) by rat explants. Explants from wild-type mice responded similarly. Explants from nNOS-/- mice had higher basal AVP secretory rate in response to 1 pM IRL 1620: 271 +/- 48 compared with 150 +/- 24% basal x explant(-1) x h(-1) (P < 0.05) from wild-type murine explants. In the nNOS-/-, SNP suppressed stimulated release, and L-NAME exerted no additional stimulatory effect: 243 +/- 38% basal x explant(-1) x h(-1). Thus nitric oxide inhibits the AVP secretory response induced by ET(B) receptor activation within the hypothalamo-neurohypophyseal system and is generated primarily by the nNOS isoform. The modulation of AVP secretion by ET and also nitric oxide can take place independently from their effects on cerebral blood flow, systemic hemodynamics, or the arterial baroreflex.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0363-6119
pubmed:author
pubmed:issnType
Print
pubmed:volume
290
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R1208-15
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16357097-Animals, pubmed-meshheading:16357097-Dose-Response Relationship, Drug, pubmed-meshheading:16357097-Endothelins, pubmed-meshheading:16357097-Enzyme Inhibitors, pubmed-meshheading:16357097-Hypothalamo-Hypophyseal System, pubmed-meshheading:16357097-Male, pubmed-meshheading:16357097-Mice, pubmed-meshheading:16357097-Mice, Inbred C57BL, pubmed-meshheading:16357097-Mice, Knockout, pubmed-meshheading:16357097-NG-Nitroarginine Methyl Ester, pubmed-meshheading:16357097-Nitric Oxide, pubmed-meshheading:16357097-Nitric Oxide Synthase Type I, pubmed-meshheading:16357097-Osmolar Concentration, pubmed-meshheading:16357097-Peptide Fragments, pubmed-meshheading:16357097-Rats, pubmed-meshheading:16357097-Rats, Long-Evans, pubmed-meshheading:16357097-Receptor, Endothelin B, pubmed-meshheading:16357097-Vasopressins
pubmed:year
2006
pubmed:articleTitle
Nitric oxide modulation of ET(B) receptor-induced vasopressin release by rat and mouse hypothalamo-neurohypophyseal explants.
pubmed:affiliation
Dept. of Medicine, Wayne State Univ. School of Medicine and John D. Dingell VA Medical Center, 4160 John R #908, Detroit, MI 48201, USA. nrossi@med.wayne.edu
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, Non-P.H.S.