The ionic mechanism of phenylephrine-induced rhythmic contractions in rabbit mesenteric arteries treated with ryanodine.

Phenylephrine induces endothelium-independent rhythmic contractions in ryanodine-treated rabbit mesenteric arteries. To elucidate the ionic mechanism of this rhythmic behaviour, rabbit mesenteric arterial rings were suspended in an organ chamber for isometric tension studies. Yohimbine, propranolol, and atropine had no effect on these contractions, minimizing the possibility that transmitter release from nerve terminals was involved. Additionally, the oscillatory contractions were not altered by diphenhydramine, cimetidine, and indomethacin, thus ruling out the involvement of histamine and prostaglandins. This oscillatory response was completely abolished after the removal of extracellular Ca2+, as well as after Ca2+ channel blockade by diltiazem or nifedipine. Sparteine and quinidine, Ca(2+)-activated K+ channel blockade by diltiazem or nifedipine. Sparteine and quinidine, Ca(2+)-activated K+ channel antagonists, also abolished the oscillation. In contrast, tetraethylammonium and 3,4-diaminopyridine, voltage-dependent K+ channel antagonists, augmented the response. Glibenclamide, an antagonist of the ATP-sensitive K+ channel, had no effect on the rhythmic contractions. These results suggest that the rhythmic contractions observed in rabbit mesenteric arteries after ryanodine treatment were caused by the movement of Ca2+ and K+ across the plasmalemma via the voltage-dependent Ca2+ channel and the Ca(2+)-activated K+ channel, respectively.