The actions of quinine on the rat isolated rectum was studied. Quinine (2.5 X 10(-5) - 2.5 X 10(-4) M) initiated rhythmic phasic contractions (RPC) which were prevented by verapamil, lanthanum, indomethacin or Ca2+-withdrawal, but were unaffected by tetrodotoxin, L-propranolol, phentolamine, or atropine. Higher quinine concentrations (2.5 X 10(-4) - 10(-3) M) relaxed the rat rectum and inhibited the RPC induced by lower concentrations. Exposure to high Ca2+-Tyrode solution (6 Ca2+-Tyrode) increased the baseline tone of the muscle. Under this condition, quinine (2.5 X 10(-4) - 10(-3) M), but not lower concentrations relaxed the muscle. Quinine (2.5 X 10(-5) - 10(-3) M) concentration-dependently inhibited KCl and acetylcholine-induced contractions, but more readily blocked KCl than acetylcholine-induced responses; the inhibitory effect of quinine against KCl, but not acetylcholine, was largely reversed by increasing the Ca2+ concentration of the Tyrode solution. It is concluded that quinine-induced RPC occurred independently of adrenergic or cholinergic mechanisms, and are likely to be due to enhanced Ca2+ influx into the rectum, while the relaxation encountered with higher concentrations may be due to inhibition by quinine of transmembranal Ca2+ influx. Evidence was obtained that quinine may preferentially inhibit Ca2+ influx through a pathway linked to high K+ depolarisation.
Acetylcholine Animals