Linked Life Data

1891338

Source:http://linkedlifedata.com/resource/pubmed/id/1891338

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1991-10-17
pubmed:abstractText
Using the patch-clamp technique, we have characterised the inward current from enzymatically dispersed rabbit pulmonary arterial cells, and investigated the effects of the vasodilator, nitroprusside (NP), on these and other membrane currents. With Cs(+)-filled pipettes, inward currents were recorded during brief depolarizing voltage steps in both physiological Ca2+ and 10 mM Ba2+. The threshold for current activation was positive to -40 mV and the current peaked at 0 mV for Ca2+ and +10 mV for Ba2+. During the first few minutes of recording, inward currents increased or "ran-up". This could not be attributed to blockade of outward current or the inclusion of adenosine triphosphate (ATP) in the patch pipette. Experiments revealed that all the inward current was carried through a single type of voltage-activated Ca2+ channel, namely the high-threshold, dihydropyridine-sensitive channel. It was unaffected by tetrodotoxin but was abolished at all potentials by low concentrations of Cd2+ (100 microM) or nifedipine (1-2 microM). NP (1 microM) suppressed peak inward Ba2+ current at +10 mV by approximately 45%. Higher concentrations (50 microM) did not produce further blockade of the current. This decrease was associated with increased inactivation of the current, and both effects required the presence of ATP in the patch pipette. In physiological Ca2+, using K(+)-filled pipettes, NP was found to induce spontaneous bursts of outward currents, which are probably activated by the release of Ca2+ from Ca(2+)-overloaded stores. These results are consistent with NP lowering cytosolic Ca2+, and hence causing vasodilation, by inhibiting Ca2+ influx through voltage-gated Ca2+ channels and by promoting Ca2+ uptake into the sarcoplasmic reticulum.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
418
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
462-70
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Modulation of calcium movements by nitroprusside in isolated vascular smooth muscle cells.
pubmed:affiliation
Department of Pharmacology, United Medical School, St Thomas's Hospital, London, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't