The Pressor Effect of Tyramine in Man and Its Modification by Reserpine Pretreatment*

Abstract

Reserpine has been shown to cause depletion of catecholamines in various isolated tissues and in pharmacological preparations of intact animals (1)(2)(3)(4)(5). Several aspects of the alterations in body function associated with administration of reserpine to man have been reported: in two schizophrenics who had received reserpine, de la Lande and associates (6) showed that ephedrine infused into the brachial artery had no effect on forearm blood flow; Westfall and Watts (7) showed that in normal students there was a diminished response of blood pressure and finger temperature to smoking after fourteen days of reserpine administration; Burger (8) found diminished plasma norepinephrine levels, and Gaddum, Krivoy, and Laverty (9) and Carlsson, Rasmussen, and Kristjansen (10) described decreased urinary excretion of catecholamines after long term reserpine administration. However, there appear to be no formal studies in man showing that reserpine affects cardiovascular responses, as has been postulated to explain the circulatory collapse which may occur in patients who have received reserpine and are subjected to anesthesia ( 11 ) and shock therapy (12). Depletion of the tissue stores of norepin'ephrine should result in a reduced pressor effect of tyramine, as this is believed to be due entirely to release of endogenous norepinephrine (13-14). MATERIAL AND METHODSTwelve male patients aged 37 to 73 were studied (Table I). They had all been in-patients for a considerable time and were free of obvious cardiovascular disease, ascites, and peripheral neuropathy. They were not receiving reserpine, sympathomimetic amines, or monamine oxidase inhibitors.The subject lay comfortably on a couch, and polyethylene catheters were placed in the brachial artery on one side and a forearm vein on the other. Blood pressure was recorded continuously with a Sanborn capacitance manometer model no. 267B or a Statham resistance manometer model no. 23B4 and a Sanborn recorder model no. 150M. In some studies, the blood pressure was electrically meaned, in others an instantaneous recording was obtained and mean arterial pressure (MAP) estimated by the formula MAP = diastolic blood pressure plus % pulse pressure. Cardiac outputs (CO) were estimated by dye dilution with indocyanine green, a Colson cuvette densitometer model no. 110 I.R., and Harvard pump model 600-900. Duplicate determinations of CO before injections of tyramine gave 95% confidence limits for the method of + 0.64 L per mm. Total peripheral resistance (TPR) was calculated from the formula TPR (dyne-seccm') =80 X MAP (mm Hg)/CO (L per minute).

Idiopathic postural hypotension: physiologic observations and report of a new mode of therapy

“…Further, the vasoconstriction observed during tyramine infusion suggested that the postganglionic sympathetic nerves contained norepinephrine. Both animal (20) and human studies (21,22) indicate that the hemodynamic effects of tyramine are due to its ability to release norepinephrine from sympathetic nerve endings.…”

Effect of Reserpine on Sympathetic Vasoconstrictor Responses

“…While some studies reported partial or complete inhibition of the Valsalva overshoot (1,2 ) and mild orthostatic hypotension (3) this has not been confirmed by other investigators (4-6). Investigations of the effects of reserpine on vasoconstrictor responses have produced variable results.…”