Hemodynamic Effects of Verapamil in Essential Hypertension at Rest and During Exercise

Summary In recent years the calcium antagonist verapamil has been used in the treatment of essential hypertension. Relatively little work has been done to elucidate its long‐term haemodynamic effects at rest and during exercise. Ten males with previously untreated essential hypertension in WHO stage I, aged 35–55 years, were studied on an outpatient basis. Oxygen consumption, heart rate, cardiac output (Cardiogreen) and intra‐arterial brachial pressure were recorded at rest in the supine and sitting position and during steady state work at 50,100 and 150 W. As expected, the hypertension was associated with an increase in total peripheral resistance. The subjects were treated with verapamil 120–240 mg daily as the sole drug for one year. The haemodynamic study was then repeated. One subject demonstrated a slight increase in blood pressure at rest and during exercise, while there was a blood pressure reduction in the other 9. The nonresponding patient was excluded from the statistical evaluation. The main results were as follows: There was a statistically significant reduction in systolic, diastolic and mean arterial pressure at rest as well as during exercise. The reductions reached about 10% at rest, slightly less during exercise. The blood pressure reduction was associated with a statistically significant reduction in total peripheral resistance at rest only. During exercise, the reduction in resistance was modest (about 5%). The heart rate was practically unchanged during supine rest, but decreased about 8% at rest sitting and during exercise. The stroke volume was increased 11% at rest sitting (p < 0.05) and also tended to be increased during exercise, but the changes were not statistically significant. The cardiac index was practically unchanged. It is concluded that the blood‐pressure reduction induced by longterm treatment with verapamil is due to a reduction in total peripheral resistance, no significant change in cardiac index, and a slight decrease in heart rate compensated by an increase in stroke index. This haemodynamic profile differs from the haemo‐dynamic changes induced by long‐term treatment with beta‐blockers.