Linked Life Data

8898688

Source:http://linkedlifedata.com/resource/pubmed/id/8898688

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1996-12-11
pubmed:abstractText
The interaction between ATP-sensitive K+ channels (KATP) and nitric oxide (NO) was studied in pial arterioles of piglets. We examined the effects of N omega-nitro-L-arginine methyl ester (L-NAME), a general inhibitor of nitric oxide synthase (NOS), and 7-nitroindazole (7-NI), a selective inhibitor of neuronal NOS, on aprikalim-induced cerebral vasodilation. Topically applied, aprikalim, a selective activator of KATP, dilated arterioles by 11 +/- 7% at 10(-8) M and 17 +/- 6% at 10(-6) M. After L-NAME treatment (15 mg/kg, i.v.), the response was reduced (4 +/- 4% and 12 +/- 7%, respectively; n = 8, p < 0.05). Administration of 7-NI (50 mg/kg, i.p.) did not change pial arteriolar responsiveness to aprikalim. However, both L-NAME and 7-NI reduced the vasodilator responses to 10(-4) M N-methyl-D-aspartate (NMDA) (by 73% and by 36%, respectively). Furthermore, 7-NI treatment abolished the glutamate-induced dilatation of pial arterioles. Administration of L-NAME reduced the NOS activity in the cerebral cortex by 88%, whereas the reduction after the 7-NI treatment was 44%. Pre-treatment and coadministration of 10(-5) M glibenclaminde, a specific inhibitor of KATP or L-NAME administration, did not change the dilatory response to sodium nitroprusside. We conclude that NO may be involved in aprikalim-induced dilation of pial arterioles.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0271-678X
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1158-64
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Interaction between ATP-sensitive K+ channels and nitric oxide on pial arterioles in piglets.
pubmed:affiliation
Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27157-1083, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.