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Mechanism of uridine 5′‐triphosphate‐induced Ca(2+) waves in rat basilar artery
Author(s) -
Syyong Harley,
Kuo KuoHsing,
van Breemen Casey
Publication year - 2007
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.21.6.a1157
Subject(s) - ryanodine receptor , cyclopiazonic acid , biophysics , extracellular , endoplasmic reticulum , chemistry , basilar artery , stimulation , intracellular , medicine , endocrinology , biochemistry , biology
Uridine 5′‐triphosphate (UTP) is a potent vasoconstrictor and induces Ca 2+ waves in cerebral arteries. We investigated the mechanism of UTP‐induced Ca 2+ waves in rat basilar artery using the Ca 2+ ‐sensitive dye Fluo‐4 and confocal microscopy. UTP elicits cyclic increases in intracellular Ca 2+ which progressively decrease in amplitude and correspond to transient force generation. Initiation of Ca 2+ waves is dependent on Ca 2+ release from the sarcoplasmic reticulum (SR), as blockade of the sarco(endo)plasmic reticulum Ca 2+ ‐ATPase with cyclopiazonic acid abolishes Ca 2+ waves. Their initiation is not affected by inhibition of inositol 1,4,5‐triphosphate receptors with 2‐aminoehoxydiphenylborinate, but depletion of the ryanodine‐sensitive Ca 2+ stores by caffeine preincubation prior to UTP stimulation abolishes the Ca 2+ waves. Finally, although blockade of L‐type voltage‐gated Ca 2+ channels (L‐VGCCs) does not affect Ca 2+ waves, removal of extracellular Ca 2+ significantly decreases their duration. These findings suggest that Ca 2+ waves in rat basilar artery are linked to force generation and are due to repetitive cycles of Ca 2+ release from the ryanodine‐sensitive component of the SR, but extracellular Ca 2+ influx through channels other than L‐VGCCs is important for their maintenance, presumably by supplying Ca 2+ for SR refilling. This work was funded by the Canadian Institutes for Health Research.