It has been known that carbachol increases intracullular sodium activity(a_N^i_a) and twich force. However the mechanism of a_N^i_a increase is not clear.
The a_N^i_a twich force and membrane potenital guinea pig papillary muscle were measured simulta...
It has been known that carbachol increases intracullular sodium activity(a_N^i_a) and twich force. However the mechanism of a_N^i_a increase is not clear.
The a_N^i_a twich force and membrane potenital guinea pig papillary muscle were measured simultaneously during exposure to carbachol(3X10exp(-4)M) and subsquent washout in the absence and presence of selective NaH exchange inhibitor, hexamethylene amiloride, or low extracellular pH(6.6) condition. The results are :
1. Hexamethylene amiloride(30㎛) inhibited NH_4Cl(10mM) induced transient decrease of a_N^i_a following marked increase of a_N^i_a which indicates that hexamethylene amiloride is a Na-H exchange inhibitor of heart muscle.
2. Carbachol induced a_N^i_a increase in quiescent and beating ventricular muscle were inhibited by hexamethylene amiloride.
3. Low extracelluar pH(6.6) inhibited carbachol indeced a_N^i_a increase in quiescent and beating ventricular muscle.
4. Low extracellular pH increased twitch force, increased action potential duration and intracellular sodium activity, and depolarized diastolic membrance potental.
From above results, it is suggested that carbachol increase a_N^i_a via Na-H exchange and Na-H exchange system of ventricular muscle which is different form the action of muscarinic receptor stimulation in Purkinje fibers.