Exercise training produces numerous adaptations in the coronary circulation
, including an increase in coronary tone, both in conduit and resistance ar
teries. On the basis of the importance of voltage-gated Ca2+ channels (VGCC
) in regulation of vascular tone, we hypothesized that exercise training wo
uld increase VGCC current density in coronary smooth muscle. To test this h
ypothesis, VGCC current was compared in smooth muscle from conduit arteries
(>1.0 mm), small arteries (200-250 mu m), and large arterioles (75-150 mu
m) 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 inve
rsely related to arterial diameter, i.e., large arterioles > small arteries
> conduit arteries. Exercise training increased peak inward currents appro
ximately twofold in smooth muscle from all arterial sizes compared with tho
se from Sed (large arteriole, -12.52 +/- 2.05 vs. -5.74 +/- 0.99 pA/pF; sma
ll 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). Dihydropyridi
ne sensitivity, voltage dependence, and inactivation kinetics identified th
is Ca2+ current to be L-type current in all arterial sizes from both Sed an
d Ex. Furthermore, peak VG;CC 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 enduranc
e exercise training. This increased VGCC density may provide an important m
echanistic link between functional and cellular adaptations in the coronary
circulation to exercise training.