Mechanisms of tetraethylammonium-induced contraction in the canine coronary artery.

Tetraethylammonium chloride (TEA) at concentrations over 10(-3) mol/l produced a concentration-dependent contraction in the isolated canine coronary artery. We investigated mechanisms of the contractile response and the effects of various vasodilators on the contraction. While phentolamine, propranolol, guanethidine, atropine and tetrodotoxin did not affect the TEA response, the response was attenuated by a reduction in the extracellular potassium concentration and was augmented by an increase in the concentration of potassium. The response was also augmented by other potassium conductance blockers (CsCl and 4-AP). On the other hand, the contractile response to phenylephrine used as a control drug was not affected by the extracellular potassium concentration or by CsCl. Verapamil or removal of extracellular calcium abolished the TEA, but not the phenylephrine response. Nicorandil, isoproterenol, adenosine or glyceroltrinitrate produced an equipotent relaxation in the coronary arteries contracted by TEA and by phenylephrine, whereas acetylcholine relaxed to a lesser extent the arteries contracted by TEA than those contracted by phenylephrine. These results suggest that the TEA-induced contractions are strictly dependent on the reduction of potassium conductance and extracellular calcium while the phenylephrine-induced contractions are not and that the relaxing effects of tested vasodilators, except for acetylcholine, may not be affected by such different contractile mechanisms.