α- and β-adrenergic mechanisms mediate blood pressure control by norepinephrine and angiotensin in ducks

Adrenergic mechanisms for the pressor actions of blood-borne l-norepinephrine (NE) and fowl angiotensin II (ANG II) were studied in barbiturate-anesthetized adult ducks (Anas platyrhynchos). NE (1.5-6.0 nmol · kg^-1) or ANG II (0.4-1.6 nmol · kg^-1) injected iv caused dose-dependent increases in mean arterial pressure (P_a) and pulse pressure (P_p) but slowed cardiac frequency (f_H); higher doses of ANG II increased P_a, P_p, and f_H. β-Adrenergic blockade by propranolol lowered baseline P_a, completely blocked cardiovascular responses to isoproterenol, augmented the bradycardic effect of NE, and inhibited the stimulation of P_p by ANG II. However, the tachycardiac effect of high-dose ANG II persisted during β-blockade. α-Adrenergic blockade following iv prazosin completely blocked the pressor effect of methoxamine, diminished the pressure response to NE, and decreased P_a sensitivity to ANG II injections. Combined α- and β-adrenergic blockade decreased both the sensitivity and the maximal P_a response to ANG II. We conclude that (i) β-adrenergic mechanisms predominate in the maintenance of resting P_a, (ii) NE increases P_a principally by α-adrenergic action while β-adrenergic stimulation buffers the consequent bradycardia, and (iii) although the positive chronotropic effect of high doses of ANG II probably is not mediated by catecholamines, low doses of ANG II elevate P_a and P_p by α- and β-adrenergic mechanisms.