Original Contributions |
From the Academic Medical Center, University of Amsterdam (Netherlands), Department of Medical Physics and Cardiovascular Research Institute.
Correspondence and reprint requests to Dr E. VanBavel, Academic Medical Center, PO Box 22700, 1100 DE Amsterdam, the Netherlands. E-mail e.vanbavel{at}amc.uva.nl
AbstractPressure-induced activation
of vascular smooth muscle may involve electromechanical as well as
nonelectromechanical coupling mechanisms. We compared calcium-tone
relations of cannulated rat mesenteric small arteries during
pressure-induced activation, depolarization (16 to 46 mmol/L
K+), and
1-adrenergic stimulation (1
µmol/L phenylephrine). The intracellular calcium
concentration was expressed as the fura-2 ratio, normalized to the
maximal and minimal ratios. In order to compare activation levels at
various pressures, tone was expressed as the ratio of active wall
tension to the maximal active tension. The passive and maximal active
pressure-diameter relations needed for the calculation of tone were
determined in a separate set of experiments, using isometric loading of
cannulated vessels. Pressure steps from 20 to 60 and then to 100
mm Hg caused a modest rise of calcium. Nifedipine (1
µmol/L) blocked both the calcium rise and the resulting myogenic
responses. Electromechanical coupling could not fully account for the
myogenic response: the calcium sensitivity, defined as the slope of the
calcium-tone relation, was five times higher during pressure-induced
activation compared with potassium stimulation and twice as high as the
sensitivity during
1-adrenergic stimulation. We
therefore conclude that the myogenic response involves a small but
necessary rise in calcium due to influx through L-type calcium
channels, as well as a nonelectromechanical coupling mechanism that
greatly enhances the calcium sensitivity of the contractile
machinery.
Key Words: Ca2+ channel myogenic response vascular smooth muscle mesenteric artery rat
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