Dihydropyridine-sensitive Ca2+ influx modulated by stretch in A7r5 vascular smooth muscle cells.
We examined 45Ca2+ influx in A7r5 vascular smooth muscle cells under cyclical stretch and static conditions and compared the results obtained at resting membrane potential (2.5 mM [K+]o, Em = -58 mV according to uptake of [3H]tetraphenylphosphonium) with those under depolarizing conditions (70 mM [K+]o, Em = -27 mV). Application of 10% average strain (24% maximum) in cycles of 3 s on, 3 s off at resting Em caused a 5-fold increase in Ca2+ influx rate to a level similar to depolarized cells and depolarized, stretched cells. 1 mu M (+)-isradipine blocked 90% of the stretch- or depolarization-activated Ca2+ uptake. When the cells were stretched under Na+ -free conditions, a reduction, not activation, of Ca2+ influx rate occurred. Our results suggest that stretching of cultured aortic vascular smooth muscle cells enhances Ca2+ uptake through a voltage-dependent, dihydropyridine-sensitive Ca2+ entry pathway, whose activation by stretch is dependent upon extracellular Na+.
Department of Physiology, Tulane University School of Medicine, New Orleans, LA 70112-2699, USA.
V
V
Ruiz-Velasco
M B
MB
Mayer
L J
LJ
Hymel
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000502:physiology; D002460:Cell Line; D004095:Dihydropyridines / Q000494:pharmacology; D008564:Membrane Potentials; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D051381:Rats; D012964:Sodium / Q000502:physiology; D013314:Stress, Mechanical
D015220:Calcium Channels; D004095:Dihydropyridines; D012964:Sodium; D002118:Calcium