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The relationship between the action potential, intracellular calcium and force in intact phasic, guinea‐pig uretic smooth muscle
Author(s) -
Burdyga T. V.,
Wray Susan
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.00867.x
Subject(s) - biophysics , contraction (grammar) , chemistry , calcium , muscle contraction , plateau (mathematics) , electrophysiology , myosin , medicine , endocrinology , biology , organic chemistry , mathematical analysis , mathematics
1 We investigated the relationship between the action potential, Ca 2+ and phasic force in intact guinea‐pig ureter, following physiological activation. 2 The action potential elicited a Ca 2+ 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. 3 Prolongation of the plateau, by agonists, prolonged the third component of the Ca 2+ transient and increased force amplitude and duration. 4 The force‐Ca 2+ relationship during phasic contractions showed hysteresis; more force was produced as Ca 2+ declined than when it rose. Paired pulse stimuli suggested that the delay between Ca 2+ 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 Ca 2+ but significantly increased the delay, suggesting that myosin phosphorylation is a major contributor to it. 5 Prolongation of the duration of the [Ca 2+ ] i transient, at unchanged amplitude, increased force. The rise of [Ca 2+ ] i did not limit the rate of contraction. Slowing of the rate of [Ca 2+ ] i rise abolished the hysteresis between Ca 2+ and force. 6 Cooling reduced force, increased the delay and hysteresis between Ca 2+ and force, but did not affect the rate of rise of Ca 2+ . The reduction in force could be compensated, by increasing the duration of the Ca 2+ transient. 7 We suggest that in vivo , steady‐state force‐Ca 2+ relationships are not applicable in phasic smooth muscles. Furthermore, agonists increase force mainly by prolonging the action potential, which increases the duration of the [Ca 2+ ] signal.