Calcium blockers may reduce contractility of vascular smooth muscle as well as that of myocardial cells. Therefore, falls in both total peripheral vascular resistance (TPR) and cardiac output (CO) might be responsible for a fall in blood pressure (BP) caused by calcium blockers in essential hypertension. We have studied the acute and chronic haemodynamic effects of nisoldipine (a new calcium blocker) in 19 patients with essential hypertension at rest in the supine and sitting positions and during 100-W dynamic exercise to investigate whether CO might be compromized by acute and chronic calcium blockade. Intra-arterial pressure, CO (by Cardiogreen), stroke volume, heart rate and TPR were measured hourly after the first dose of 10 mg nisoldipine (acute study) and then after 1 year of nisoldipine treatment (mean dose 25 mg; chronic study). The maximal first dose response was seen after 1 h, i.e. a fall in intra-arterial pressure (9%) and TPR (19%) and a reflex rise in heart rate (9%) and CO (12%). The effects levelled off during the next 2 h. After 1 year of treatment there was a more marked reduction in BP: at rest intra-arterial pressure fell (14% supine, 16% sitting) due to fall in TPR (19%) but without significant changes in heart rate or CO; during 100-W exercise, intra-arterial pressure fell (14%) due to reduction in both TPR (7%) and CO (6%). In conclusion, nisoldipine lowers BP by reducing TPR, both acutely and chronically. The initial reflex tachycardia and rise in CO disappear during long-term treatment, probably due to resetting of the baroreceptors. After chronic treatment a small reduction in CO contributes to the hypotensive effect during exercise. Since the filling pressure was not measured it is not known whether this is due to a small negative inotropic effect or to other mechanisms.