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With the aim of evaluating the antihypertensive action and the antioxidant properties of amlodipine and nifedipine-GITS, a group of 41 patients were enrolled in a double blind, comparative, parallel study. Patients initially received identical placebo during 4 weeks; then active treatment during 6 weeks; amlodipine 5 mg daily (20 patients; 49.0 Ϯ 8.1 years) and nifedipine-GITS, 30 mg daily (21 patients 49.2 Ϯ 8.4 years).At the end of placebo and active phases, serum determinations of malondialdehyde (MDA) by colorimetric thiobarbituric acid method were carried out in each patient.Office systolic/diastolic blood pressure [standard error] were reduced by amlodipine in 24 Ϯ 2.2/16 Ϯ 1.7 mmHg from 164 Ϯ 3.3/103 Ϯ 1.27 mmHg; nifedipine GITS reduced it in 23 Ϯ 2.63/16 Ϯ 1.5 mmHg from 166 Ϯ 3.4/104 Ϯ 1.2 mmHg (p Ͻ 0.001 both). Heart rate increased an average of 1.4 bpm in amlodipine group (p ϭ 0.48), and 4.7 bpm in nifedipine group (p ϭ 0.021).Serum MDA was reduced in 34.01 Ϯ 7.2 nM (15.3%) from 221.8 Ϯ 14.9 nM in the amlodipine group (p ϭ 0.034); meanwhile nifedipine GITS group serum malondialdehyde was increased in 6.42 Ϯ 16.6 nM from 221.08 Ϯ 14.9 nM without statistical significance (p ϭ 0.694).In conclusion, monotherapy with amlodipine or nifedipine GITS reduced blood pressure at the same level after 6 weeks of antihypertensive treatment. Heart rate was slightly increased by nifedipine. Serum MDA was significantly reduced only by amlodipine indicating important antioxidant activity. Inhibition of serum malondialdehyde by amlodipine may contribute to mechanisms of atheroprotection; as well as, protection of myocardial ischemic injury.Key Words: Amlodipine; Nifedipine GITS; Malondialdehyde The rise in blood pressure in response to L-NAME infusion has been attributed to inhibition of nitric oxide (NO)-induced vasodilation accompanied by sympathetic stimulation. To evaluate the neurohormonal response to NO synthase (NOS) inhibition in man, 7 normal young (age 26 Ϯ 2 years) volunteers were given cumulative infusions of L-NAME (1.5 to 5 mg/kg) and monitored over 4 -6 hours. Blood pressure rose variably (systolic 114 to 125 p Ͻ .05, mean 81 to 92, P Ͻ .01; diastolic 66 to 76, mmHg p Ͻ .01). Heart rate fell (mean 63 to 57, P Ͻ .01). Plasma norepinephrine (HPLC) decreased consistently (mean 191 to 82 pg/ml, P Ͻ 0.01) and plasma renin activity usually fell (0.93 to 0.55 ng/ml/hr, P ϭ NS). Plasma endothelin (ET 1 ) was unchanged.There was a trend for the rise in pressure in response to L-NAME to correlate with less neurohormonal suppression (r 2 ϭ .79). Thus L-NAME infusion is associated with inhibition rather than stimulation of the neurohormonal contribution to vascular tone. Variability in blood pressure response to NOS inhibition appears to reflect variability in the neurohormonal response. Hypertension may therefore represent an imbalance between endothelial and neurohormonal control of vascular tone. In the forearm circulation, there is evidence that African Americans (AA) demonstrate reduced vasodilation in response to...

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