Involvement of different activator Ca(2+) in the rate-dependent stretch-induced contractions of canine basilar artery.

Abstract

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 Ca(2+)-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 Ca(2+) concentration ([Ca(2+)](i)) and active tension. The contraction in response to slow stretch (1 mm/s) was abolished by nicardipine and Gd(3+). Quick stretch (100 mm/s) increased [Ca(2+)](i) and active tension, both of which were partially inhibited by nicardipine or Gd(3+). The Gd(3+)-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 Ca(2+) influx through L-type voltage-dependent Ca(2+) channels (VDCs), whereas the quick stretch-induced contraction was dependent on Ca(2+) release from sarcoplasmic reticulum (SR) and Ca(2+) influx through L-type VDCs.