| pubmed-article:6619512 | pubmed:abstractText | The effects of sympathetic and parasympathetic nerve stimulation on resistance to flow in the proximal urethra was examined in male, chloralose-anesthetized cats. Hypogastric (sympathetic) nerve stimulation increased urethral resistance, an effect that was blocked by the alpha-adrenergic antagonist prazosin (0.1 mg/kg), reduced 50% by ganglionic blockade with hexamethonium (0.4 to 0.6 mg/min) and potentiated by the beta-adrenergic antagonist sotalol (5 mg/kg). In the presence of phenylephrine-induced constrictions of the urethra, hypogastric nerve stimulation decreased resistance by a sotalol-sensitive, hexamethonium-resistant mechanism. The results imply that sympathetic stimulation can either raise or lower urethral resistance under different conditions, and that the organization of the nerves mediating the two types of response differs. Because pelvic nerve stimulation produced small and inconsistent responses, the parasympathetic input was instead activated by sacral ventral root stimulation. Sacral stimulation produced an atropine-sensitive constriction when basal urethral resistance was low, and dilatation when resistance was high. The latter response was reduced by atropine, but was resistant to sotalol. However, the decrease in resistance produced by acetylcholine in the presence of PE was not reduced by atropine, implying that acetylcholine-induced dilatation of the urethra is not due to activation of muscarinic receptors on smooth muscle. It is hypothesized that parasympathetic dilatation of the urethra may be mediated by a non-cholinergic, non-adrenergic inhibitory transmitter released from post-ganglionic neurons. A muscarinic mechanism may be involved in this response either to potentiate the action of the unknown transmitter or to facilitate the ganglionic excitation of these neurons. Parasympathetic constrictor responses can be attributed to activation of postganglionic cholinergic neurons. | lld:pubmed |
