A B S T R A C T The mechanism of postarrhythmic renal vasoconstriction was studied in 28 dogs anesthetized with pentobarbital sodiumiii (30 mg/kg i.v.). Rapid atrial or ventricular pacinig or induction of' atrial fibrillationi were tised to produce at least a 20% prompt decrease in cardiac output and meani arterial blood pressure. Return to control cardiac output and blood pressure occurred within 3 min after cessation of the arrhythmia, but renal blood flow remained significantly decreased (26%) with gradual recovery by 17.7+6.6 min Infusion of phentolamine (0.25 mg/mmiin) into the renal artery, intravenous hexamethonium (1 mg/kg), adrenal demedullation, or cooling the cervical vagi prevented postarrhythmic renal vasoconstriction. In contrast, renal denervation, intravenous bretylium (10 mg/kg), intravenous atropine (0.5 mg/kg) or intrarenal SQ 20881 (0.20 mg/min) had no effect on postarrhythmic renal vasoconstriction. Intravenous propranolol (0.5 mg/kg) intensified postarrhythmic renal vasoconstriction. These data suggested that the postarrhythmic renal vasoconstrictive response re(Iuired intact vagi and was due to alpha adrenergic stimulation by adrenal catecholamiines. However, femoral arterial catecholamiinie levels were not elevated above control during postarrhythmiic renal vasoconistriction. '