Bicarbonate ion modulates the function of the voltage-dependent calcium channel in the smooth muscle of the rat vas deferens.
Bicarbonate dependence of Bay K 8644 effects in rat vas deferens warrants no clinical extrapolation; leaves open its modulation of voltage-dependent calcium channels for further study.
Effects of Bay K 8644. partial depolarization with high potassium, and nifedipine on the dose-response curves of the rat vas deferens to norepinephrine, methacholine and KCl were investigated in HEPES-buffered physiological salt solution (PSS) with or without 20 mM sodium bicarbonate. In the bicarbonate-containing PSS, Bay K 8644 at 10-6 M enhanced the maximal contractions in response to norepinephrine, methacholine and KCl by 31.4, 103.3 and 40.1%, respectively. In the bicarbonate-free PSS, where the maximal contractions induced by norepinephrine, methacholine and KCl were 77.5, 75.0 and 68.2% of those in the bicarbonate-containing PSS, respectively, Bay K 8644 did not enhance the maximal contractile response to any of the agonists, although the contractions induced by low concentrations of KCl were increased by Bay K 8644. Increasing the potassium concentration in the PSS from 6 to 20 mM enhanced the maximal contractions in response to norepinephrine and methacholine in the bicarbonate-containing PSS, whereas in the bicarbonate-free PSS, the treatment decreased the contractions. In the two PSSs, nifedipine similarly inhibited the contraction in response to either 10-6 M norepinephrine or 68 mM KCl. These results suggest that bicarbonate ion modulates the function of the voltage-dependent calcium channel in the smooth muscle of the rat vas deferens.
No takes yet. Share an insight, caveat, or question.
SUZUKI et al. (1990) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: