Linked Life Data

9820899

Source:http://linkedlifedata.com/resource/pubmed/id/9820899

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-3-1
pubmed:abstractText
We tested the hypothesis that the negative metabolic effects of elevating cyclic GMP act through inhibition of L-type calcium channels in quiescent cardiac myocytes. The steady state O2 consumption (VO2) of ventricular myocytes, isolated from hearts of New Zealand white rabbits, was measured in a glass chamber using Clark-type oxygen electrodes. The cellular cyclic GMP levels were determined by radioimmunoassay at baseline with either 0.5 mM or 2.0 mM of Ca2+, sodium nitroprusside at increasing concentration (10(-8),(-6),(-4) M) with and without pretreatment by BAY K8644 10(-5) M (L-type Ca2+ channel activator) in 0.5 mM Ca2+, or nitroprusside with and without pretreatment with nifedipine 10(-4) M (L-type Ca2+ channel blocker) in 2.0 mM Ca2+. In the 0.5 mM Ca2+ medium, basal VO2 was 459 +/- 104 (nl O2/min per 10(5) myocytes) with a corresponding cyclic GMP level of 112 +/- 23 (fmol/10(5) myocytes). With nitroprusside 10(-4) M, VO2 was decreased to 285 +/- 39 and cyclic GMP level was significantly elevated to 425 +/- 128. In the same medium, VO2 was slightly increased by BAY K8644 10(-5) M while the cyclic GMP level did not change. With BAY K8644 10(-5) M, nitroprusside 10(-4) M decreased VO2 and increased cyclic GMP to a level which was similar to cells treated with nitroprusside alone. In the 2.0 mM Ca2+ medium, the basal VO2 and cyclic GMP were 518 +/- 121 and 137 +/- 24. In the presence of nitroprusside 10(-4) M, VO2 was decreased to 295 +/- 49 and cyclic GMP was increased to 454 +/- 116. In the same medium, nifedipine 10(-4) M significantly decreased VO2, while the cyclic GMP level was comparable to the baseline. After nifedipine 10(-4) M, nitroprusside 10(-4) M decreased VO2 and increased cyclic GMP to levels which were similar to control. Therefore, in quiescent cardiac myocytes, the negative metabolic effects associated with cyclic GMP were not primarily mediated through inhibition of L-type Ca2+ channels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0300-9130
pubmed:author
pubmed:issnType
Print
pubmed:volume
198
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
123-32
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Negative metabolic effects of cyclic GMP in quiescent cardiomyocytes are not related to L-type calcium channel activity.
pubmed:affiliation
Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway 08854-5635, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't