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Intravenous injections of guanfacine (1 microgram-3 mg/kg) elevated dose-dependently blood pressure in adrenalectomized, pitched rats. The vasopressor activity of guanfacine was weaker than those of clonidine, an alpha 2-agonist and 1-phenylephrine, an alpha 1-agonist. However, the maximal response produced by guanfacine was the same as that produced by clonidine, while it was much smaller than that produced by 1-phenylephrine. The dose-response curve to guanfacine for increase in blood pressure was shifted in a parallel fashion to the right by 1 mg/kg of yohimbine, an alpha 2-antagonist and by 1 mg/kg of phentolamine, a nonselective alpha 1- and alpha 2-antagonist. However, 0.1 mg/kg of prazosin, a selective alpha 1-antagonist, produced an inhibition of the blood pressure rise induced by higher doses of guanfacine, but not that induced by lower doses. Guanfacine (1 microgram-1 mg/kg) inhibited dose-dependently the tachycardia induced by electrical stimulation of spinal nerves at C7-Th1 in adrenalectomized, pithed rats. The maximal inhibition by guanfacine of heart rate increase induced by electrical stimulation was about 60%. These inhibitory effects were antagonized by yohimbine and phentolamine, but not by prazosin. These results indicate that guanfacine is an alpha 2-agonist with approximately equal potency towards the pre- and postsynaptic alpha 2-adrenoceptors, just as clonidine is, but is weaker as an alpha 2-agonist than clonidine.

The relevance of the type of detrusor sphincter dyssynergia (DSD) and motor unit analysis as examined by simultaneous recordings of electromyography (EMG) of the external urethral sphincter (EUS) and bladder pressure was discussed in the first report. In this report, they were analysed similarly before and after radical transurethral resection of the prostate (TUR-P) to see how it was effective in relieving DSD. Furthermore, the response of the EUS to alpha-adrenergic stimulation was examined by analyzing its motor unit activity. Radical TUR-P was performed in 18 cases. After radical TUR-P, there was an improvement in the type of DSD (3 cases) or in its sub-types (8 cases), associated with decrease in residual urine rate in 16 cases. EUS responded to alpha-adrenergic stimulation with an increase in the frequency of pre-existing motor units and recruitment of new motor units. After radical TUR-P,EUS was similarly activated when stimulated with alpha-adrenergics. These data indicated that radical TUR-P was effective in relieving DSD by suppressing or abolishing abnormal continence reflex. Moreover, alpha-adrenergic activation of EUS also seemed to suggest a possible sympathetic role in the genesis of DSD, although exact mode of its involvement in the somatomotor innervation of the EUS remains to be settled.