Alpha- and beta-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 X kg-1) or ANG II (0.4-1.6 nmol X kg-1) injected iv caused dose-dependent increases in mean arterial pressure (Pa) and pulse pressure (Pp) but slowed cardiac frequency (fH); higher doses of ANG II increased Pa, Pp, and fH X beta-Adrenergic blockade by propranolol lowered baseline Pa, completely blocked cardiovascular responses to isoproterenol, augmented the bradycardic effect of NE, and inhibited the stimulation of Pp by ANG II. However, the tachycardiac effect of high-dose ANG II persisted during beta-blockade. alpha-Adrenergic blockade following iv prazosin completely blocked the pressor effect of methoxamine, diminished the pressure response to NE, and decreased Pa sensitivity to ANG II injections. Combined alpha- and beta-adrenergic blockade decreased both the sensitivity and the maximal Pa response to ANG II. We conclude that (i) beta-adrenergic mechanisms predominate in the maintenance of resting Pa, (ii) NE increases Pa principally by alpha-adrenergic action while beta-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 Pa and Pp by alpha- and beta-adrenergic mechanisms.