Debrisoquin is a post-ganglionic sympathetic blocker.1 It increases accumulation of the monoamine oxidase (MAO) substrate l-m-octopamine in isolated rabbit heart when used at a concentration of 1 mM.2 Debrisoquin reduces norepinephrine levels in the left and right atrium and ventricles, as well as the mesenteric and femoral arteries in anesthetized dogs when administered at a dose of 5 mg/kg per day for seven days.3 Debrisoquin decreases mean aortic pressure, heart rate, and total peripheral vascular resistance in the same model.
|1. Heffernan, A.G.A., and Carty, A.T. Clinical observations on the use of debrisoquine sulphate (declinax) in the treatment of hypertension. I. J. Med. Sc. 3(1), 37-43 (1970).|2. Giachetti, A., and Shore, P.A. Monoamine oxidase inhibition in the adrenergic neuron by bretylium, debrisoquin, and other adrenergic neuronal blocking agents. Biochem. Pharmacol. 16, 237-238 (1966).|3. Cavero, I., Gerold, M., Saner, A., et al. The cardiovascular effects of the antihypertensive drug debrisoquin: A contribution to the pharmacology of chronic treatment. I. one-week administration to dogs. J. Pharmacol. Exp. Ther. 206(1), 123-131 (1978).