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Department of Medical Physiology, Texas A & M University System Health Science Center, College Station, Texas 77843
Stretch-activated ion currents were
recorded from vascular smooth muscle (VSM) after enzymatic isolation
of single cells from porcine coronary arterioles. Patch pipettes were
used to record whole cell current and control cell length. Under
voltage clamp in physiological saline solution, an inward cation
current (ICAT) was activated by
105-135% longitudinal stretch. ICAT
coincided with an increase in intracellular Ca2+
concentration. Under current clamp, membrane depolarization was induced
by stretch. The magnitude of ICAT varied from
0.8 to 6.9 pA/pF at a holding potential of 60 mV.
ICAT was graded with stretch, inactivated on
release, and could be repeatedly induced. A potassium current
(IK) activated in unstretched cells by
depolarization was also enhanced by stretch. In Ca2+-free
bath solution, stretch-induced enhancement of IK
was blocked, but ICAT was still present.
Hexamethyleneamiloride (50 µM), a reputed inhibitor of
mechanosensitive channels, blocked ICAT and the
stretch-induced increase in IK but not basal
IK. Grammostolla spatulata venom
(1:100,000) blocked basal IK, blocked
stretch-induced increases in IK, and blocked
ICAT. Iberiotoxin, a specific
Ca2+-activated K+ channel blocker, did not
alter ICAT but blocked the stretch-induced increase in IK and increased the magnitude of
stretch-induced depolarization. We concluded that longitudinal stretch
directly activates a cation current and secondarily activates a
Ca2+-activated K+ current in isolated coronary
myocytes. Although these two currents would partially counteract each
other, the predominance of ICAT at physiological
potentials is likely to explain the depolarization and contraction
observed in intact coronary VSM during pressure elevation.
mechanosensitive channels; vascular myogenic response; calcium-activated potassium channels
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