Involvement of Different Activator Ca²⁺ in the Rate-Dependent Stretch-Induced Contractions of Canine Basilar Artery

抄録

Stretch evoked a contraction in a rate-dependent manner in canine basilar artery; slow stretch at rates less than 3 mm/s produced no active tension, whereas quick stretch at rates over 5 mm/s did. Large conductance Ca²⁺-activated K⁺ channel blockers, including charybdotoxin, iberiotoxin, and tetraethylammonium (TEA) sensitized the basilar artery to mechanical stimulation. TEA shifted the stretch rate-tension relationship toward the left. Thus, in the presence of TEA, the slow stretch (0.1-3 mm/s) could increase in intracellular 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 thapsigargin, but not by nicardipine. Ryanodine, cyclopiazonic acid, thapsigargin, U-73122, and calphostin C also abolished the nicardipine-insensitive component of quick stretch-induced contraction. These results suggest that the slow stretch-induced contraction was exclusively dependent on the Ca²⁺ influx through L-type voltage-dependent Ca²⁺ channels (VDCs), whereas the quick stretch-induced contraction was dependent on Ca²⁺ release from sarcoplasmic reticulum (SR) and Ca²⁺ influx through L-type VDCs.