HAeMODYNAMIC BASIS OF ACUTE PRESSOR REACTIONS AND HYPERTENSION

Abstract

To be the first Haile Selassie lecturer is a unique privilege. My pleasure at having been chosen for this task has two further causes. The first is that we I am going to summarize work that I have been carrying out with my colleagues Dr. Fencl, Hejl, and Jirka over the past eight years when we have been interested in the question of the relation between acute rises of blood pressure during pressor reactions of various kind and the permanent rise of blood pressure forming the basis of essential hypertension. Hines (1940) and others have claimed that some subjects with a normal pressure respond to a standardized cold stimulus by an exaggerated and protracted blood pressure rise and that the incidence of later essential hypertension is much more frequent among these hyper-reactors than among normal subjects. Although the far-reaching conclusions of Hines were disproved by further investigations (Hoobler, 1961; our own unpublished data), there isno doubt that many candidates for later permanent hypertension react to various pressor stimuli in the way suggested by Hines, but the connexion between these temporary rises of blood pressure and permanent hypertension was not established. The question naturally arose whether these transient exaggerated pressor responses could not actually be already an early phase of hypertension, the permanent blood pressure elevation being produced by fusion of the protracted acute rises.If this were so, it would be expected that the blood pressure would be increased both acutely and in essential hypertension by the same hcmodynamic mechanism. It is today generally accepted that in essential hypertension this increase is due to a rise of the total peripheral vascular resistance, while cardiac output remains normal. Data are scarce on the hemodynamic basis of acute blood pressure elevations, but Stead et al. (1945) have shown that during anxiety accompanying cardiac catheterization, blood pressure is increased by an increase in cardiac output, while total peripheral vascular resistance is unchanged or low. Thus it appears that there is no link between the acute and chronic blood pressure rise.

Responses to mental stress and physical provocations before and during long term treatment of hypertensive patients with beta‐adrenoceptor blockers or hydrochlorothiazide.

“…Mental stress elicits a circulatory reaction similar to that evoked by the hypothalamic defence reaction (Brod, 1963;Folkow, 1982). Mental stress reduces systemic vascular resistance and evokes vasodilatation in skeletal muscle whether elicited by an arithmetic test (Brod, 1963) or by the stressor used in the present study (Hjemdahl et al, 1984).…”

“…Mental stress reduces systemic vascular resistance and evokes vasodilatation in skeletal muscle whether elicited by an arithmetic test (Brod, 1963) or by the stressor used in the present study (Hjemdahl et al, 1984). Even though sympathetic activation is intimately involved in the cardiovascular response to mental stress, only minor elevations of venous plasma noradrenaline are seen (Folkow et al, 1983;Hjemdahl et al, 1984).…”

Mental stress opposes endothelium-dependent vasodilation in young healthy individuals

“…[10][11][12]16,17 These different haemodynamic patterns are reflected by differences in circulating catecholamine levels. The mental arithmetic test mainly induced a rise in circulating epinephrine levels, while the cold pressor test mainly caused an elevation of circulating norepinephrine.…”

Beta‐adrenoceptor blockade and psychic stress in man. A comparison of the acute effects of labetalol, metoprolol, pindolol and propranolol on plasma levels of adrenaline and noradrenaline.

“…However, most studies on the cardiovascular and hormonal response to psychic stress have been carried out by exposing the subjects to rather unpleasant situations of frustration, anger or fear (Brod, 1963;Bonelli etal., 1979).…”