MECHANISM OF THE ARTERIAL HYPERTENSION INDUCED BY PAREDRINOL (α-N-DIMETHYL-p-HYDROXYPHENETHYLAMINE

Abstract

Paredrinol produces in normal subjects a type of acute arterial hypertension that closely resembles that observed in disease. The avg. duration of the hypertension after the intramusc. injection of 25 mgm. of paredrinol is 1 hr. The tendency to a slower heart rate, vigorous apex impulse, loud heart sounds, and hypertension itself are the only outstanding abnormalities produced by the drug. There is no significant change in blood flow in the foot, forearm, and calf. The cardiac output, circulation time, and basal metabolism are not significantly altered. The blood flow in the dilated hand is moderately decreased. The spontaneous fluctuations in vasomotor tone in the hand and foot are decreased. The venous tone in the hand is increased. The venous pressure is increased by from 30 to 40 mm. of water. The T-waves in the electrocardiogram become higher. These changes are usually not great enough to be detectable unless the resting values for the particular subject are known. The decrease in heart rate results from an increase in vagal tone caused by stimulation of the carotid sinus and aortic nerves, since if the vagal effect is removed by atropine, paredrinol causes an increase rather than a decrease in heart rate. The combination of nitrite and tilting to the upright position pools sufficient blood to reduce the paredrinol hypertension to normal. Thus, if the arterial blood pressure rises to alarming heights, or if headache develops, the hypertension can be rapidly and permanently reduced. The hypertension produced by paredrinol may result from either or both of the following mechanisms (1) A primary increase in peripheral resistance from a direct vasoconstrictor effect on the minute vessels (arterioles, capillaries, venules); (2) a primary increase in venous tone and an emptying of the splanchnic reservoirs, causing increased venous return to the heart and a secondary increase in peripheral resistance.