Ca2+ sequestration as a determinant of chaos and mixed-mode
dynamics in agonist-induced vasomotion.
Griffith, T M, & D H Edwards.
Departments of Diagnostic Radiology and *Cardiology, Cardiovascular
Sciences Research Group, University of Wales College of Medicine,
Heath Park, Cardiff, UK, CF4 4XN
APStracts 3:0515H, 1996.
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+-ATPase pump of
the sarcoplasmic reticulum, first induced then abolished highly
characteristic mixed-mode oscillatory behaviour. 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 KCa channels, and by ouabain, which
blocks the Na+-K+ ATPase. We conclude that there is nonlinear
crosstalk 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.
Received 9 September 1996; accepted in final form 15 November
1996.
APS Manuscript Number H814-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996