Vagally mediated bradycardiac effect of prazosin in anaesthetized rats

Prazosin at doses of 100 or 1000 nmol/kg i.v. induced bradycardia in urethane-anaesthetized rats. The bradycardia was completely abolished by atropine pretreatment or vagotomy. Prazosin also stimulated gastric acid secretion. This effect was completely abolished by vagotomy. The maximal hypotensive effect after prazosin i.c.v. occurred 10 min later than with i.v. administration. It is concluded that prazosin possesses vagal a stimulating property that may in part explain its modest tachycardiac effect seen in clinical use. The mechanism of vagal stimulation by prazosin remains unclear. The present findings suggest that prazosin does not exert any direct effects on central vagal structures accessible from the ventricular space.