HAeMODYNAMIC BASIS OF ACUTE PRESSOR REACTIONS AND HYPERTENSION

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Abstract
During acute blood pressure rises in response to unpleasant emotions or a cold stimulus, blood is shifted from the viscera and skin to muscle. Total peripheral vascular resistance may drop or increase according to the prevalence of the vasodilator (muscular) or vasoconstrictor (visceral) component of this reaction. An increase in cardiac output is an integral part of this reaction and is superseded by a decrease only in those instances where total peripheral vascular resistance increases greatly. This hemodynamic reaction is analogous to that produced by strenuous muscular exercise or by its verbal suggestion. Similar reactions were observed in animals during an orientation reflex, rage reaction, or on stimulation of a hypothalamic area. It is suggested that preparation of the circulation for strenuous muscular exercise is the common denominator and that in adult men preparation to severe muscular action (fight or flight) takes place during unpleasant emotions, though any visible muscular action is suppressed by social inhibition. Similarly, as with hypothalamic stimulation, the efferent vasoconstrictor pathway of the emotional hemodynamic reaction in man lies in the adrenergic sympathetic fibre and can be blocked by dibenamine, the vasodilator pathway to muscle in the cholinergic sympathetic, and can be partly blocked by atropine or by stellate ganglion anaesthesia. Metabolic studies of muscle during emotion and muscular exercise show that muscular hyperemia during emotion is not called forth by increased metabolic demands and is obviously a component of a centrally co-ordinated preparation of the circulatory system to strenuous exercise. This is further documented by the fact that the extra blood during the emotional muscle hyperemia bypasses the capillary bed as suggested by studies of the slope of the disappearance curve of KI131 from muscle. Under resting conditions general and regional hemodynamic changes in subjects with essential hypertension are analogous to those observed in normal subjects during emotion. It is suggested that this might be due to the protracted nature of the acute pressor responses and that the starting point of essential hypertension might be a faulty regulation of one of the basic hemodynamic reactions that is mobilized many times during the day under ordinary conditions of life.