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1 Worcester Foundation for Experimental Biology, Shrewsbury, Massachusetts
Serotonin in the range of 0.01 to 1000µg (per 40 ml) produced dose-related contractions of normal and chronically sympathetically and parasympathetically denervated isolated iris sphincters of the cat. In larger doses, it elicited contractions of smaller amplitude and shorter duration followed by longlasting relaxation. Higher doses of serotonin desensitized the preparation to subsequent administration of this compound. After an initial phase of attenuation, serotonin augmented and prolonged the electrically-induced phase of sphincter contraction. Several observations suggested that this was due either to interaction of serotonin with the alpha-adrenergic component of the electrically-induced contraction or to the action of serotonin as a " false transmitter." The electrically-induced relaxation phase gradually decreased to reach smallest values at the time when serotonin-induced sphincter contractions were maximally enhanced. Methysergide, 1 mg, markedly decreased serotonin-induced sphincter contractions but did not attenuate the electrically-induced phase of sphincter contraction, thus indicating that serotonin has no transmitter function in the iris sphincter. Phenoxybenzamine and morphine, in doses comparable to those used by Gaddum and collaborators, did not appreciably attenuate the effect of serotonin on this preparation.
Submitted on June 24, 1966