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ULTRASTRUCTURAL BASIS OF ASYNCHRONOUS URIDINE 5′‐TRIPHOSPHATE (UTP)‐INDUCED CA(2+) WAVES IN RAT BASILAR ARTERY
Author(s) -
Syyong Harley,
Yang Clarice,
Trinh Gina,
Kuo KuoHsing,
Breemen Cornelis
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.913.1
Subject(s) - ryanodine receptor , biophysics , extracellular , endoplasmic reticulum , chemistry , calcium , basilar artery , intracellular , medicine , biology , biochemistry , organic chemistry
A common form of Ca2+ signaling in smooth muscle cells is Ca2+ oscillations. We observed that uridine 5′‐triphosphate (UTP) elicits cyclic, dose‐dependent increases in intracellular Ca2+ which underlie tonic force generation in rat basilar artery, similar to those observed in conduit arteries. We also observed subplasmalemmal junctions between the plasma membrane (PM) and sarcoplasmic reticulum (SR), known as PM‐SR junctions. Pharmacological dissociation of these junctions abolishes maintenance of Ca2+ waves, but does not affect Ca2+ release. The maintenance of Ca2+ waves is dependent on extracellular Ca2+ entry, which is mediated by L‐type voltage‐gated calcium channels (L‐VGCCs), non‐selective cation channels (NSCCs), and by the plasma membrane Na+/Ca2+ exchanger (NCX) working in reverse‐mode. Blockade of inositol 1,4,5‐triphosphate receptors (IP3Rs), but not ryanodine receptors, abolishes ongoing Ca2+ waves. These findings suggest that Ca2+ waves in rat basilar artery underlie tonic force generation and are due to repetitive cycles of Ca2+ release from the IP3Rs, and that extracellular Ca2+ influx through L‐VGCCs, NSCCs, and reverse‐mode NCX is important for their maintenance by supplying Ca2+ for SR refilling. Finally, despite its similarity to resistance vessels, the basilar artery behaves like a conduit artery with respect to the mechanism of Ca2+ waves. This work was funded by CIHR of Canada.