Afterload reduction by nifedipine--the acute haemodynamic response to exercise in hypertensive subjects

In 16 people with essential hypertension, heart rate (HR), bloodpressure (BP) and relative cardiac volumes were measured atrest and during submaximal upright exercise before and after10 mg of sublingual nifedipine using radionuclide ventriculography. In 10 patients who had had no previous therapy (BP 152/103±5/3mmHg) nifedipine produced a fall in BP of 6/12±3/3 mmHg(SEM) and a rise in HR of 15±5 bpm (P<0.001). Thiswas associated with a rise in LVEF of 0.07±0.02 (P<0.005)and in cardiac output of 44±9%, presumably as a resultof ventricular offloading. The cardiac response to exercisegiven the different starting values, was unchanged by nifedipine.Thus the HR was 101±6 bpm at rest after nifedipine andon exercise rose to 124±6 bpm (P<0.001): stroke volumewas +22±8% at rest after nifedipine and rose to +43±12%on exercise. Thus cardiac output which had increased by 44±9%after nifedipine increased by 100±10% from the initialvalue. In 6 patients pre-treated with atenolol (100 mg) and with similarresting BP (158/101±5/4 mmHg) there was a fall in BPof 32/15±3/2 mmHg after nifedipine which was greaterthan in the previously untreated group (P<0.01). In thisgroup HR increased by 8±3 bpm (P<0.05). Followingnifedipine the exercise response was similar given the differentstarting values. The combination of nifedipine and a beta adrenoceptor antagonistcan depress myocardial function and the difference between pressure–volumeratios in the two groups supports this view but there was noimportant depressant effect. We conclude that the combinationof beta blocker and nifedipine therapy is effective and safein hypertensive subjects without significant myocardial dysfunction.