Involvement of different activator Ca2+ in the rate-dependent stretch-induced contractions of canine basilar artery

Stretch evoked a contraction in a rate-dependent manner in canine basilar a rtery; slow stretch at rates less than 3 mm/s produced no active tension, w hereas quick stretch at rates over 5mm/s did. Large conductance Ca2+-activa ted K+ channel blockers, including charybdotoxin, iberiotoxin, and tetraeth ylammonium (TEA) sensitized the basilar artery to mechanical stimulation. T EA shifted the stretch rate-tension relationship toward the left, Thus, in the presence of TEA, the slow stretch (0,1-3mm/s) could increase in intrace llular Ca2+ concentration ([Ca2(+)](i)) and active tension. The contraction in response to slow stretch (1 mm/s) was abolished by nicardipine and Gd3. Quick stretch (100 mm/s) increased [Ca2+](i) and active tension, both of which were partially inhibited by nicardipine or Gd3+. The Gd3+-insensitive component of quick stretch-induced contraction was eliminated by thapsigar gin, but not by nicardipine. Ryanodine, cyclopiazonic acid, thapsigargin, U -73122, and calphostin C also abolished the nicardipine-insensitive compone nt of quick stretch-induced contraction. These results suggest that the slo w stretch-induced contraction was exclusively dependent on the Ca2+ influx through L-type voltage-dependent Ca2+ channels (VDCs), whereas the quick st retch-induced contraction was dependent on Ca2+ release from sarcoplasmic r eticulum (SR) and Ca2+ influx through L-type VDCs.