STRESS-INDUCED CHANGES IN BLOOD-PRESSURE AND LEFT-VENTRICULAR FUNCTION IN MILD HYPERTENSION

Left ventricular function was studied by M-mode 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 (6.0 +/- 0.3 vs. 5.0 +/- 0.3 L/min), which was related to elevations of stroke volume and heart rate (73 +/- 2 vs. 66 +/- 2 beats/min). 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 (15 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 similarity 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 activation 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.