AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 283: H2169-H2176, 2002; doi:10.1152/ajpheart.00603.2002
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Vol. 283, Issue 6, H2169-H2176, December 2002

SPECIAL TOPICS
Alkaline pH shifts Ca2+ sparks to Ca2+ waves in smooth muscle cells of pressurized cerebral arteries

Thomas J. Heppner1,*, Adrian D. Bonev1,*, L. Fernando Santana2, and Mark T. Nelson1

1 Department of Pharmacology, University of Vermont College of Medicine, Burlington, Vermont 05405-0068; and 2 Department of Physiology and Biophysics, University of Washington, Seattle, Washington 98195

The effects of external pH (7.0-8.0) on intracellular Ca2+ signals (Ca2+ sparks and Ca2+ waves) were examined in smooth muscle cells from intact pressurized arteries from rats. Elevating the external pH from 7.4 to 7.5 increased the frequency of local, Ca2+ transients, or "Ca2+ sparks," and, at pH 7.6, significantly increased the frequency of Ca2+ waves. Alkaline pH-induced Ca2+ waves were inhibited by blocking Ca2+ release from ryanodine receptors but were not prevented by inhibitors of voltage-dependent Ca2+ channels, phospholipase C, or inositol 1,4,5-trisphosphate receptors. Activating ryanodine receptors with caffeine (5 mM) at pH 7.4 also induced repetitive Ca2+ waves. Alkalization from pH 7.4 to pH 7.8-8.0 induced a rapid and large vasoconstriction. Approximately 82% of the alkaline pH-induced vasoconstriction was reversed by inhibitors of voltage-dependent Ca2+ channels. The remaining constriction was reversed by inhibition of ryanodine receptors. These findings indicate that alkaline pH-induced Ca2+ waves originate from ryanodine receptors and make a minor, direct contribution to alkaline pH-induced vasoconstriction.

ryanodine receptors; voltage-dependent calcium channels; arterial diameter

* T. J. Heppner and A. D. Bonev contributed equally to this study.




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