Glibenclamide, glipizide, and phentolamine increased coronary perfusion pressure in guinea-pig isolated hearts, suggesting vasoconstriction may result indirectly from vasoactive mediator release.
Do K+-channel blockers increase coronary perfusion pressure in guinea-pig isolated hearts?
Glibenclamide-induced coronary vasoconstriction in guinea-pig hearts may be partially mediated by the indirect release of vasoactive mediators.
Glibenclamide, glipizide and phentolamine, three drugs which have been reported to block ATP-dependent potassium channels, increased the coronary perfusion pressure in guinea-pig isolated hearts perfused at constant flow. Blockers of other types of potassium channels, 4-aminopyridine and UK-66,914, did not significantly increase perfusion pressure. Exposing hearts to a single concentration of 3 microM glibenclamide caused a greater degree of vasoconstriction than when this was preceded by lower concentrations. The 3 microM glibenclamide-induced vasoconstriction was reduced by prazosin (1 microM), mepyramine (0.1 microM) and ranitidine (10 microM) but not by a combination of mepyramine and ranitidine or by ritanserin (0.01 microM). These results suggest that a component of the vasoconstriction induced by glibenclamide may result indirectly from the release of vasoactive mediators.
Gwilt et al. (Thu,) conducted a other in Coronary vasoconstriction. K+-channel blockers (glibenclamide, glipizide, phentolamine) vs. 4-aminopyridine and UK-66,914 was evaluated on Coronary perfusion pressure. Glibenclamide, glipizide, and phentolamine increased coronary perfusion pressure in guinea-pig isolated hearts, suggesting vasoconstriction may result indirectly from vasoactive mediator release.