Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3 Pt 2
pubmed:dateCreated
1991-4-11
pubmed:abstractText
It has been suggested that cromakalim (BRL 34915)-induced vasorelaxation was associated with stimulation of ATP-sensitive K channels. The hyperpolarization resulting from activation of this mechanism might then inhibit voltage-dependent Ca2+ entry and subsequent contraction. The present study evaluated the similarities of 42K efflux stimulated by ATP depletion (verified by high-performance liquid chromatography) and by exposure to cromakalim (10 microM) in rabbit superior mesenteric arteries. Both depletion of intracellular ATP and exposure to cromakalim significantly stimulated 42K efflux (P less than 0.05). Glyburide (a selective inhibitor of ATP-sensitive K channels in pancreatic beta-cells) inhibited 42K efflux stimulated by ATP depletion and by cromakalim exposure. Glyburide (10 microM) had no significant effect on either basal 42K or the 42K efflux stimulated by norepinephrine and by K depolarization, which cause voltage and Ca2(+)-dependent activation of K channels. Glyburide therefore had a relatively selective effect on vascular smooth muscle. The glyburide-sensitive 42K efflux during ATP depletion and exposure to cromakalim was greatest in Ca2(+)-free solution (Mg raised to 10 mM). We conclude that in vascular smooth muscle both depletion of ATP and exposure to cromakalim stimulate 42K efflux via a glyburide-sensitive mechanism with properties similar to those of ATP-sensitive K channels observed in cardiac and pancreatic beta-cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
260
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H848-54
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Stimulation of arterial 42K efflux by ATP depletion and cromakalim is antagonized by glyburide.
pubmed:affiliation
Department of Physiology, University of Missouri School of Medicine, Columbia 65212.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't