AJP - Heart and Circulatory Physiology, Vol 272, Issue 4 1696-H1709, Copyright © 1997 by American Physiological Society

ARTICLES

Ca2+ sequestration as a determinant of chaos and mixed-mode dynamics in agonist-induced vasomotion

T. M. Griffith and D. H. Edwards
Department of Diagnostic Radiology, University of Wales College of Medicine, Cardiff, United Kingdom.

We have investigated the contribution of smooth muscle Ca2+ stores to chaotic vasomotion in isolated rabbit ear resistance arteries. In preparations constricted by histamine, exposure to cyclopiazonic acid (CPA) and thapsigargin (TSG), which inhibit the Ca2+-adenosinetriphosphatase (ATPase) pump of the sarcoplasmic reticulum, first induced then abolished highly characteristic mixed-mode oscillatory behavior. The fractal dimension of the vasomotion, which reflects the minimum number of contributing dynamic variables, remained between 2 and 4 until the point at which oscillations disappeared completely. By contrast, ryanodine, which attenuates Ca2+-induced Ca2+ release, decreased the fractal dimension of the responses to <2 in a graded concentration-dependent fashion by selectively suppressing a slow subcomponent of the overall rhythmic activity. CPA-associated oscillations were insensitive to ryanodine but could be abolished by verapamil and modulated in an inhibitory or stimulatory fashion by charybdotoxin, which blocks Ca2+-activated K+ channels, and by ouabain, which blocks the Na+-K+-ATPase. We conclude that there is nonlinear cross talk between CPA/TSG-sensitive Ca2+ stores and a membrane oscillator that regulates Ca2+ influx and that the kinetics of Ca2+ uptake by the CPA/TSG-sensitive pool can be distinguished dynamically from the kinetics of Ca2+ release from its ryanodine-sensitive subcomponent.

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