Calcium and the contractility of arterial smooth muscle

Abstract

The contraction of an isolated arterial segment (500 µ o.d.) was measured as a reduction in flow through its lumen at a constant perfusing pressure. The stimulating agents used to induce contraction were high K+, norepinephrine, and Pitressin. Contraction due to these agents was first abolished after 15 min of perfusion with zero [Ca++]0, then it was re-established by a series of perfusions containing increasing [Ca++]0. During this procedure, high K+ contraction reappeared at 0.5 mmoles/liter [Ca++]0 and increased in proportion to [Ca++]0. Drug contraction, however, reappeared as a near maximal response between 0.5 and 0.75 mmoles/ liter [Ca++]0 and increased relatively little with larger elevations of [Ca++]0. Simultaneous reduction in [Na+]0 potentiated the re-established K+ contraction but had no effect on the re-established norepinephrine contraction. These differences in the Ca++-contractility relationship for drugs and K+ depolarization suggest Ca++ is utilized differently by the two modes of stimulation to bring about contraction.