We have, in the present work, studied the importance of the kidneys and the renal hypotensive agent, medullipin, in modulating the blood pressure (BP) response to bradykinin, as well as their ability to influence the balance between the NO- and the adrenergic systems superimposed on a bradykinin-induced hypotension. 2. The rats were pretreated with the NO-synthase inhibitor, N omega-nitro-L-arginine methyl esther (L-NAME) (0.3 g kg-1), proadifen (50 mg kg-1), an inhibitor of the medullipin-system, and nephrectomy (24 h) (Nx) alone, and L-NAME in combination with proadifen, Nx or phentolamine (2 mg kg-1). Subsequent injections of bradykinin (3, 6, 15, 30 micrograms kg-1) induced an acute hypotensive response. The fall in BP was dose-dependent in all groups (P < 0.01), except in the Nx/L-NAME group. No differences in the fall in BP were observed between the groups. 3. The duration of the hypotensive response was abbreviated after L-NAME-treatment (P < 0.05). Proadifen-treatment and Nx had no significant effect on the duration of the hypotension in control rats or in L-NAME-treated rats. Pretreatment with phentolamine prevented the L-NAME-induced rapid restoration of BP (P < 0.001). 4. In L-NAME-treated rats a transient hypertension followed the bradykinin-induced hypotensive response. This hypertensive response was not observed after Nx or proadifen-treatment alone, and addition of Nx or proadifen to L-NAME treatment did not alter the hypertensive response as compared to L-NAME alone. Phentolamine, however, abolished the L-NAME-induced hypertension (P < 0.05). 5. In conclusion, the present results do not support the involvement of the medullipin-system or other hypotensive systems localized in the kidneys, in modulating and counteracting the compensatory adrenergic response following an acute bradykinin-induced hypotension. A hampering modulating effect of the NO-system on this compensatory adrenergic response was confirmed, indicating a close relationship between these two systems in BP homeostasis.
