SUMMARY The antihypertensive effect of diltiazem (180-270 mg/day) and nifedipine (40-60 mg/day) in slow-release forms was assessed over 8 weeks in a double-blind parallel study in 40 subjects with essential hypertension at rest and during exercise. Blood pressure was comparably reduced in both groups at rest as well as during exercise. The responder rates (2:10% reduction in diastolic blood pressure) after 8 weeks of therapy were 53% at rest and 75% during exercise in the diltiazem group and 78% and 50%, respectively, in the nifedipine group. Diltiazem decreased heart rate by 8% (p<0.01), while nifedipine did not affect it. As a consequence, myocardial oxygen consumption, as judged by the pressure-rate product, was reduced by diltiazem. Resting plasma norepinephrine levels were increased significantly after 8 weeks of diltiazem therapy. Plasma epinephrine, renin, aldosterone, glucose, insulin, and lactate and routine laboratory parameters were unchanged at the end of the study. No significant changes in total cholesterol and triglyceride levels were observed after 8 weeks. Whereas therapy with diltiazem resulted in an 8% fall in low density lipoprotein cholesterol after 8 weeks (p<0.05), nifedipine induced a drop in very low density lipoprotein cholesterol (p<0.05) after 8 weeks of therapy. We conclude that both diltiazem and nifedipine are effective antihypertensive agents lacking undesirable metabolic side effects. Diltiazem, however, had the advantage of lowering heart rate and myocardial oxygen consumption. Therefore, the use of drugs with a direct dilating effect on the arterial wall is a logical treatment approach.2 As demonstrated more than 15 years ago by Bender 3 and Brittinger et al., 4 calcium entry blockers have an antihypertensive effect. All calcium entry blockers decrease the influx of extracellular Ca 2+ and promote systemic vasodilation. The effects on myocardium, cardiac cells, and vascular smooth muscle differ depending on the drug used. While verapamil and diltiazem act on myocardium, pacemaker cells, and vascular smooth muscle, nifedipine and its derivatives act mostly at the vascular site rather than on the cardiac pacemaker.5 "

No abstract