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Stimulation of hypogastric nerve contracts the urinary bladder. Exogenous norepinephrine and dopamine cause only an insignificant contraction or relaxation, whereas tyramine regularly contracts the bladder. Denervation or pharmacological sensitization by imipramine or cocaine does not alter the minor response to norepinephrine but the latter procedure enhances the effect of hypogastric stimulation. UML 491, a serotonin blocking agent, does not affect the hypogastric nerve-bladder response, whereas phentolamine has variable effects. Dihydroergotamine causes marked spontaneous contractions. Under certain conditions reserpine, syrosingopine and α-methylmetatyrosine diminish but never block the contraction induced by sympathetic stimulation. Choline-2,6-xylyl ether bromide markedly increases spontaneous contractions of the bladder, enhances the contractions to pelvic stimulation but irregularly diminishes those to hypogastric stimulation. Only guanethidine and bretylium block the hypogastric nerve-bladder response completely and selectively. Single pretreatment with syrosingopine (10 mg/kg i.V.), α-MMT (100 mg/kg i.v.) and guanethidine (15 mg/ kg i.v.) lowers the NE concentration of the bladder (18 hr) to approximately one third of that in controls, whereas the 5-HT content remains unchanged. The NE and 5-HT concentration in the untreated bladder is 1.13±0.48and0.20±0.03 μg/g respectively. Eserine augments and hexamethonium diminishes the sympathetically induced contraction.

Summary The spontaneous and hypothalamically evoked discharge patterns of the preganglionic cervical sympathetic, splanchnic and vagal nerves have been described and discussed as potential indicators of central “autonomic tone” in cat. Chlorpromazine and diazepam, in i.v. doses of 0·3-3 mg/kg, generally reduced slightly spontaneous evoked impulse traffic in cervical sympathetic fibers, but markedly attenuated the electrical activity in splanchnic nerves. Vagal efferent activity was more subtly affected by these two agents. Pentobarbital (3–10 mg/kg i.v.) depressed spontaneous and evoked potentials in the sympathetic and vagal nerves. In addition, it prevented the poststimulatory inhibition observed in sympathetic nerves.