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The relationship between the action potential, intracellular calcium and force in intact phasic, guinea-pig uretic smooth muscle

T. V. Burdyga and Susan Wray

We investigated the relationship between the action potential, Ca²⁺ and phasic force in intact guinea-pig ureter, following physiological activation.

The action potential elicited a Ca²⁺ transient consisting of three components: a fast increment, associated with the first action potential spike, a slower increment, associated with subsequent spikes and the initial part of the plateau component, and a steady-state phase associated with the plateau.

Prolongation of the plateau, by agonists, prolonged the third component of the Ca²⁺ transient and increased force amplitude and duration.

The force-Ca²⁺ relationship during phasic contractions showed hysteresis; more force was produced as Ca²⁺ declined than when it rose. Paired pulse stimuli suggested that the delay between Ca²⁺ and force was not due to mechanical properties. Wortmannin, which has been shown to selectively inhibit force and myosin light chain (MLC) phosphorylation in the guinea-pig ureter, did not affect electrical activity or Ca²⁺ but significantly increased the delay, suggesting that myosin phosphorylation is a major contributor to it.

Prolongation of the duration of the [Ca²⁺]_i transient, at unchanged amplitude, increased force. The rise of [Ca²⁺]_i did not limit the rate of contraction. Slowing of the rate of [Ca²⁺]_i rise abolished the hysteresis between Ca²⁺ and force.

Cooling reduced force, increased the delay and hysteresis between Ca²⁺ and force, but did not affect the rate of rise of Ca²⁺. The reduction in force could be compensated, by increasing the duration of the Ca²⁺ transient.

We suggest that in vivo, steady-state force-Ca²⁺ relationships are not applicable in phasic smooth muscles. Furthermore, agonists increase force mainly by prolonging the action potential, which increases the duration of the [Ca²⁺] signal.

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