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Vascular Biology Laboratory, Dalton Cardiovascular Research Center, Departments of Physiology and Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211
Exercise
training produces numerous adaptations in the coronary circulation,
including an increase in coronary tone, both in conduit and resistance
arteries. On the basis of the importance of voltage-gated
Ca2+ channels (VGCC) in regulation
of vascular tone, we hypothesized that exercise training would increase
VGCC current density in coronary smooth muscle. To test this
hypothesis, VGCC current was compared in smooth muscle from conduit
arteries (>1.0 mm), small arteries (200-250 µm), and large
arterioles (75-150 µm) from endurance-trained (Ex) or sedentary
miniature swine (Sed). After 16-20 wk of treadmill training, VGCC
current was determined using whole cell voltage-clamp techniques. In
both Ex and Sed, VGCC current density was inversely related to arterial
diameter, i.e., large arterioles > small arteries > conduit
arteries. Exercise training increased peak inward currents
approximately twofold in smooth muscle from all arterial sizes compared
with those from Sed (large arteriole, 
12.52 ± 2.05 vs. 5.74 ± 0.99 pA/pF; small artery, 6.20 ± 0.97 vs. 3.18 ± 0.44 pA/pF; and conduit arteries, 4.22 ± 0.30 vs. 2.41 ± 0.55 pA/pF; 10 mM
Ba2+ external). Dihydropyridine
sensitivity, voltage dependence, and inactivation kinetics identified
this Ca2+ current to be L-type
current in all arterial sizes from both Sed and Ex. Furthermore, peak
VGCC current density was correlated with treadmill endurance in all
arterial sizes. We conclude that smooth muscle L-type
Ca2+ current density is increased
within the coronary arterial bed by endurance exercise training. This
increased VGCC density may provide an important mechanistic link
between functional and cellular adaptations in the coronary circulation
to exercise training.
voltage clamp; dihydropyridine; vascular smooth muscle; microcirculation; voltage-gated calcium channels; porcine
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