Abstract:
:In primarily cultured pig coronary smooth muscle cells, extracellular adenosine triphosphate (ATP; 10(-9) to 10(-3) M) dose-dependently increases intracellular calcium ([Ca2+]i). The [Ca2+]i transients measured by fura-2 fluorescence consist of peak and plateau phases with [Ca2+]i values of 191.84 +/- 5.67 nM (n = 10) and 91.67 +/- 1.89 nM, respectively. In Ca(2+)-free solution, the peak phases persisted, but there was a loss of the plateau response, indicating an initial ATP-stimulated intracellular Ca2+ release and a subsequent transarcolemmal Ca2+ entry. Various agonists have been used to characterize the P2 purinoceptor subtype involved in the ATP-induced Ca2+ transients. The rank order of potency was uridine triphosphate (UTP) > ATP > 2-meSATP > beta,gamma-meATP = alpha,beta-meATP = adenosine = 0. To examine the refilling of ATP-sensitive stores, four repetitive 60-s ATP responses were produced throughout with a 5-min recovery period in between. Now the ATP peaks gradually declined in Ca(2+)-free solution, indicating the emptying of the stores. If, however, Ca2+ entry was allowed in the "refilling period" (i.e., between the ATP pulses), the Ca2+ peaks could be maintained or restored, respectively. The data suggest that the ATP-dependent [Ca2+]i transients may be mediated via a UTP > ATP-activated P2Y purinoceptor subtype, mediating both an intracellular Ca2+ release and a transarcolemmal Ca2+ influx. The refilling of Ca2+ stores may occur through the unstimulated membrane after agonist stimulation. A putative pathway may be a "capacitative" Ca2+ entry induced on depletion of intracellular Ca2+ stores.
journal_name
J Cardiovasc Pharmacoljournal_title
Journal of cardiovascular pharmacologyauthors
Seiler L,Matyas S,Fleckenstein-Grün Gdoi
10.1097/00005344-199905000-00019subject
Has Abstractpub_date
1999-05-01 00:00:00pages
807-13issue
5eissn
0160-2446issn
1533-4023journal_volume
33pub_type
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