Calcium and the contractility of arterial smooth muscle

¹ Department of Anatomy, The University of British Columbia, Vancouver, Canada

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.

Key Words: positive inotropic effect • high K⁺ depolarization • drug excitation • norepinephrine • Pitressin • effect of Na⁺ on Ca⁺⁺ contractility relationships

Submitted on March 25, 1963