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Restraint causes an increase in plasma renin activity (PRA) which is not affected by pretreatment with dl-propranolol (1 mg/kg IP) or sotalol (15 mg/kg IP). These doses of β-adrenergic blocking agents are effective in suppressing the stimulation of PRA by isoproterenol. Large doses of dl-propranolol (10 mg/kg IP) and d-propranolol (5 mg/kg IP) attenuate the restraint-induced PRA increase. Adrenal demedullectomy does not affect the PRA response to restraint. Renal denervation blunts the PRA rise due to restraint, but not to direct stimulation by the β-adrenergic agonist, isoproterenol. It is concluded that the increase in PRA during restraint stress in rats is not solely dependent on an intact renal sympathetic innervation. A significant portion of this stress-induced PRA increase appears to involve a non-adrenergic mechanism.

Electrical and cholinergic (physostigmine) stimulation of the mesencephalic reticular formation (MRF) blocks ciliary nerve activity. Pentobarbitone increases the spontaneous ciliary nerve potential and lowers the threshold to electrical MRF stimulation. Atropine has no significant effect on spontaneous activity, but diminishes the response to electrical MRF stimulation and blocks the physostigmine-induced inhibition. In contrast, electrical stimulation and physostigmine activation of the MRF generally increases vagal efferent discharges and tends to induce rhythmicity or increase the rate of pre-existing rhythmicity. Pentobarbitone depresses spontaneous activity and blocks effects induced by electrical MRF stimulation. Atropine, per se, may increase, decrease, or modify vagal efferent activity, suggesting selective effects on different neuronal aggregates of the vagal system. Physostigmine-induced alterations of vagal outflow are antagonized by atropine. From these results it is concluded that the differential effect of MRF stimulation, physostigmine, atropine and pentobarbitone on the upper (ciliary) and lower (vagal) parasympathetic outflow represents the consequence of a different organization of those substrates which govern the two parasympathetic activities.

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.

Single light flashes or electrical stimulation of the optic nerve evoke a bi- or triphasic potential in the short ciliary nerves. The central conduction and transmission time (from the optic nerve to the emergence of the preganglionic autonomic oculomotor fibers) is estimated to be about 12 msec. After prior conditioning stimuli, evoked responses to subsequent test shocks are inhibited when the interval is between 15 and 30 msec. Recovery takes 120 msec or longer. This inhibitory period is prolonged by pentobarbital. CPZ, which constricts the pupil in man, enhances optically evoked ciliary potentials, whereas diazepam and pentobarbital decrease them. The CPZ effect is interpreted as a diminution of inhibitory influences on the pupilloconstrictor outflow.