The role of sodium pump in the inhibition of smooth muscle responsiveness to agonists during potassium restoration

Abstract

Summary1. Isometric contractions of cat splenic capsular smooth muscle in response to noradrenaline and histamine were recorded. 2. Removal of potassium from the bathing medium did not change the resting tension or the responsiveness to noradrenaline. Restoration of potassium inhibited responses to noradrenaline or histamine only if the muscles were stimulated with an agonist while in the K-free medium.3. This inhibition of responses to the agonists due to potassium was reversed rapidly by removing the ion or reversed slowly by prolonged exposure to the ion. The inhibition was also blocked by procedures or agents which block the sodium pump (ouabain, substitution of NaCl by LiCl), inhibit active processes (low ambient temperature) or prevent intracellular accumulation of sodium (substitution of choline for sodium). 4. It is proposed that under special circumstances such as when there is an increase in internal sodium concentration, the sodium pump is probably electrogenic and causes relaxation when activated by external potassium. In the normal muscle the pump is probably electrically neutral.

14β‐Hydroxyprogesterone binds to the digitalis receptor, inhibits the sodium pump and enhances cardiac contractility

“…Restoration of extracellular potassium is believed to re-establish the activity of the sodium pump of smooth muscle which has been sodiumloaded in potassium-free medium. Under these circumstances, the activated pump becomes electrogenic, inducing membrane hyperpolarization (Taylor et al, 1970) and relaxation (Bose & Innes, 1973;Bonaccorsi et al, 1977;Mallick et al, 1987) of muscle cells. This relaxation response was blocked and replaced by a small contraction if the muscle was first exposed to ouabagenin or 14,-OHP (Table 2); presumably, reversal by the steroids of relaxation is mediated through Na,K-ATPase inhibition.…”

14β‐Hydroxyprogesterone binds to the digitalis receptor, inhibits the sodium pump and enhances cardiac contractility

“…Restoration of extracellular potassium is believed to re-establish the activity of the sodium pump of smooth muscle which has been sodiumloaded in potassium-free medium. Under these circumstances, the activated pump becomes electrogenic, inducing membrane hyperpolarization (Taylor et al, 1970) and relaxation (Bose & Innes, 1973;Bonaccorsi et al, 1977;Mallick et al, 1987) of muscle cells. This relaxation response was blocked and replaced by a small contraction if the muscle was first exposed to ouabagenin or 14,-OHP (Table 2); presumably, reversal by the steroids of relaxation is mediated through Na,K-ATPase inhibition.…”

14β‐Hydroxyprogesterone binds to the digitalis receptor, inhibits the sodium pump and enhances cardiac contractility

“…Restoration of extracellular potassium is believed to re-establish the activity of the sodium pump of smooth muscle which has been sodiumloaded in potassium-free medium. Under these circumstances, the activated pump becomes electrogenic, inducing membrane hyperpolarization (Taylor et al, 1970) and relaxation (Bose & Innes, 1973;Bonaccorsi et al, 1977;Mallick et al, 1987) of muscle cells. This relaxation response was blocked and replaced by a small contraction if the muscle was first exposed to ouabagenin or 14,-OHP (Table 2); presumably, reversal by the steroids of relaxation is mediated through Na,K-ATPase inhibition.…”

14β‐Hydroxyprogesterone binds to the digitalis receptor, inhibits the sodium pump and enhances cardiac contractility

“…Restoration of extracellular potassium is believed to re-establish the activity of the sodium pump of smooth muscle which has been sodiumloaded in potassium-free medium. Under these circumstances, the activated pump becomes electrogenic, inducing membrane hyperpolarization (Taylor et al, 1970) and relaxation (Bose & Innes, 1973;Bonaccorsi et al, 1977;Mallick et al, 1987) of muscle cells. This relaxation response was blocked and replaced by a small contraction if the muscle was first exposed to ouabagenin or 14,-OHP (Table 2); presumably, reversal by the steroids of relaxation is mediated through Na,K-ATPase inhibition.…”