Opposite modulation by angiotensin II of alpha‐1D and alpha‐1A adrenoceptor‐mediated pressor responses in pithed rats

This study investigated the effects of captopril (CAP), an angiotensin‐converting enzyme inhibitor, on pressor responses induced by activation of alpha‐1D and alpha‐1A adrenoceptors in pithed rats. Male Wistar rats were pithed under pentobarbital anesthesia and prepared for blood pressure recording and intravenous (i.v.) drug administration. A dose‐response curve to the alpha‐1D and alpha‐1A adrenoceptor agonists, buspirone (BUS) and oxymetazoline (OXY), respectively, was built in animals that had received either saline (1ml/kg, i.v.) or an antagonist (1mg/kg, i.v.) for alpha‐1D (BMY7378; BMY) and alpha‐1A (5‐methyl‐urapidil; 5‐MU) adrenoceptors; these experiments were performed in rats pretreated with saline (1ml/kg, i.v.) or CAP (5mg/kg, i.v.). The effect of CAP was also tested on pressor responses induced by the selective alfa‐1A adrenoceptor agonist, A‐61603. CAP significantly decreased pressor responses to BUS but increased those to OXY and A‐61603. CAP strongly increased the inhibitory effect of 5‐MU and slightly increased that of BMY against BUS‐ and OXY‐induced effects. These data are consistent with the hypothesis that angiotensin II may promote, respectively, facilitation and depression of alpha‐1D and alpha‐1A adrenoceptor‐mediated pressor responses in pithed rats. This work is supported in part by a grants from CONACYT (199267) and CIC‐UMSNH (2006).