Abstract
We studied the mechanisms of pindolol-induced vasoconstrictions in isolated and perfused monkey coronary arteries. Phentolamine marginally reduced the vasoconstrictions, but bunazosin and DG 5128 did not. Diltiazem and methysergide significantly inhibited them, but atropine, diphenhydramine and cimetidine did not. Diltiazem significantly suppressed KCl-induced vasoconstrictions, but methysergide did not. These results suggest that pindolol-induced vasoconstrictions of monkey coronary arteries are mediated, at least partly, through 5-hydroxytryptamine receptors, but not through α-adrenoceptors, and that these vasoconstrictions appear to be associated with an increase of Ca2+ entry into the smooth muscle cell.
