CHANGES IN BLOOD-PRESSURE AND PLASMA-CATECHOLAMINES CAUSED BY TYRAMINE AND COLD-EXPOSURE

Tyramine may be used to stimulate endogenous norepinephrine release. Increases in blood pressure (BP) and plasma catecholamines were compared in normal volunteers during tyramine infusions and the more physiological sympathetic stimulus of cold exposure. In a 2nd study, the cardiac component of the tyramine pressor effect was assessed by measuring systolic time intervals and infusion tyramine in .beta.-blocked subjects. Tyramine, 15.0 .mu.g/kg per min for 30 min, elevated systolic BP from 122 .+-. 11 to 149 .+-. 4 mm Hg, without increasing diastolic BP or heart rate. Plasma norepinephrine rose from 0.547 .+-. 0.184 to 0.836 .+-. 0.096 ng/ml; plasma epinephrine was unchanged. Exposure for 30 min to 4.degree. C elevated both systolic BP (from 105 .+-. 8 to 116 .+-. 9 mm Hg) and diastolic BP (from 72 .+-. 4 to 81 .+-. 6 mm Hg). Along with this was a greater rise in plasma norepinephrine, from 0.357 .+-. 0.131 to 1.143 .+-. 0.393 ng/ml; plasma epinephrine was again unchanged. A single oral propranolol 160 mg dose caused approximately a 2-fold right shift in the systolic BP dose response to tyramine and blocked the tyramine-induced shortening of the presystolic ejection period. Tyramine apparently exerts its pressor effect mainly by stimulation of cardiac .beta.-receptors. This may account for the relatively small rise in plasma norepinephrine (relative to cold exposure) since the heart does not contribute a high proportion of circulating norepinephrine.