Short term administration of felodipine to spontaneously hypertensive rats reduced mean arterial pressure, due to peripheral vasodilatation. This vasodilatation is generalised, since blood flow, determined by the microsphere technique, is maintained or increased in most vascular beds despite substantial mean arterial blood pressure reduction. The resistance and mean arterial blood pressure reduction after felodipine was counterbalanced by an increase in cardiac output. In short term therapy, cardiac output increased because of an increase in both heart rate and stroke volume. Following long term administration of felodipine cardiac output remained elevated owing to an increase in stroke volume. The lack of tachycardia during long term felodipine administration was shown to be due to a rapid resetting of the baroreflex control of heart rate. The marked increase in stroke volume after long term administration is suggested to be due to regression of left ventricular hypertrophy and structural rebuilding of the heart towards that characteristic of the well-trained athlete. Thus, the haemodynamic pattern induced by short term felodipine administration, and probably also other antihypertensive drugs, will become modified by neurogenic and structural adaptations upon prolonged administration.