Stress‐induced changes in blood pressure and left ventricular function in mild hypertension

Abstract

Summary:Left ventricular function was studied by Mmode echocardiography at rest and during a mental arithmetic stress test and a cold-pressor test in 14 patients with mild hypertension and in 14 matched normotensive subjects. The elevation of blood pressure at rest in the hypertensive group (154+4/87+3 vs. 120+3/66+3 mmHg in the control group) was due mainly to a higher cardiac output (6.030.3 vs. 5.0+0.3 L/min), which was related to elevations of stroke volume and heart rate (73+2 vs. 66 + 2 beatdmin). Venous plasma catecholamines were similar in the two groups. Mental stress induced cardiac output-dependent increases in blood pressure in both groups; systemic vascular resistence tended to decrease. The relative increases in diastolic and mean arterial blood pressure were smaller in the hypertensive group (IS vs. 26% and 15 vs. 21 %, respectively), which exhibited signs of a reduced cardiac compliance, possibly related to a left ventricular hypertrophy. Mental stress elevated venous plasma adrenaline similarly in the two groups; effects on noradrenaline were small. The cold-pressor test increased blood pressure similarly in the two groups, largely due to increased systemic vascular resistence; plasma noradrenaline responses were also similar. Mental stress appears to elicit a differentiated sympathetic nerve acti- vation pattern resembling the hypothalamic defense reaction. Mild hypertension seems to be associated with increased arousal and cardiac activation at rest. However, an attenuated blood pressure reactivity to mental stress may reflect reduced stroke volume responsiveness, which is related to structural changes, as heart rate reactivity tended to be enhanced in mild hypertension.

Influence of Mental Stress on Cardiovascular Function as Evaluated by Changes in Energy Expenditure

“…Several studies have reported that the mental stress-induced increase in BP is greater in subjects with essential hypertension than in subjects with normal BP (27,28). However, whether the sensitivity of BP to mental stress differs between subjects with borderline hypertension and those with normal BP has not been determined conclusively (29)(30)(31). Our results did not show a statistically significant difference in the sensitivity of SBP to mental stress between subjects with high BP and those with normal BP.…”

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.…”

“…This hemodynamic pattern includes an increase in blood pressure, heart rate and cardiac output, vasoconstriction in the splanchnic and kidney regions, but an increased blood flow in skeletal muscle. [10][11][12] A recent study showed that local infusion of l-NMMA, a blocker of the NO synthesis, in the forearm could attenuate the increase in forearm blood flow (FBF) normally evoked by mental stress, 13 suggesting that NO plays an important role in the modulation of blood flow during mental stress. Furthermore, in the same study, local infusion of atropine also reduced the mental stress-induced increase in FBF indicating a role of cholinergic stimulation in the NOmediated increase in FBF caused by mental stress.…”

Mental Stress Impairs Endothelial Vasodilatory Function by a Beta-Adrenergic Mechanism

“…This hemodynamic pattern includes increments in blood pressure, heart rate and cardiac output, vasoconstriction in the splanchnic and kidney regions, but an increased blood flow in skeletal muscle (Eliasson et al 1983;Freyschuss et al 1988;Lindvall et al 1991). Studies have also showed that local infusion of Ng-mono-methyl-L-arginine (L-NMMA), a blocker of NO synthesis, in the forearm could attenuate the increase in forearm blood flow (FBF) normally evoked by mental stress (Cardillo et al 1997), suggesting that NO plays an important role in the modulation of blood flow during mental stress.…”