Amlodipine reduces blood pressure during dynamic resistance exercise in hypertensive patients.

This study investigated the effect of the dihydropyridine calcium channel antagonist, amlodipine, on blood pressure (BP) during resistance exercise performed at different intensities in hypertensives. Eleven hypertensives underwent 4 weeks of placebo and amlodipine (random double-blinded crossover design). In each phase, they performed knee extension exercise until exhaustion following three protocols: one set at 100% of 1 RM (repetition maximum), three sets at 80% of 1 RM, and three sets at 40% of 1 RM. Intraarterial BP was measured before and during exercise. Amlodipine reduced maximal systolic/diastolic BP values achieved at all intensities (100% = 225 ± 6/141 ± 3 vs. 207 ± 6/130 ± 6 mmHg; 80% = 289 ± 8/178 ± 5 vs. 273 ± 10/169 ± 6 mmHg; 40% = 289 ± 10/176 ± 8 vs. 271 ± 11/154 ± 6 mmHg). Amlodipine blunted the increase in diastolic BP that occurred during the second and third sets of exercise at 40% of 1RM (+75 ± 6 vs. +61 ± 5 mmHg and +78 ± 7 vs. +64 ± 5 mmHg, respectively). Amlodipine was effective in reducing the absolute values of systolic and diastolic BP during resistance exercise and in preventing the progressive increase in diastolic BP that occurs over sets of low-intensity exercise. These results suggest that systemic vascular resistance is involved in BP increase during resistance exercise, and imply that hypertensives receiving amlodipine are at lower risk of increased BP during resistance exercise than non-medicated patients.

Post-resistance exercise hemodynamic and autonomic responses: Comparison between normotensive and hypertensive men.

To compare post-resistance exercise hypotension (PREH) and its mechanisms in normotensive and hypertensive individuals, 14 normotensives and 12 hypertensives underwent two experimental sessions: control (rest) and exercise (seven exercises, three sets, 50% of one repetition maximum). Hemodynamic and autonomic clinic measurements were taken before (Pre) and at two moments post-interventions (Post 1: between 30 and 60 min; Post 2: after 7 h). Ambulatory blood pressure (BP) was monitored for 24 h. At Post 1, exercise decreased systolic BP similarly in normotensives and hypertensives (-8 ± 2 vs -13 ± 2 mmHg, P > 0.05), whereas diastolic BP decreased more in hypertensives (-4 ± 1 vs -9 ± 1 mmHg, P < 0.05). Cardiac output and systemic vascular resistance did not change in normotensives and hypertensives (0.0 ± 0.3 vs 0.0 ± 0.3 L/min; -1 ± 1 vs -2 ± 2 U, P > 0.05). After exercise, heart rate (+13 ± 3 vs +13 ± 2 bpm) and its variability (low- to high-frequency components ratio, 1.9 ± 0.4 vs +1.4 ± 0.3) increased whereas stroke volume (-14 ± 5 vs -11 ± 5 mL) decreased similarly in normotensives and hypertensives (all, P > 0.05). At Post 2, all variables returned to pre-intervention, and ambulatory data were similar between sessions. Thus, a session of resistance exercise promoted PREH in normotensives and hypertensives. Although this PREH was greater in hypertensives, it did not last during the ambulatory period, which limits its clinical relevance. In addition, the mechanisms of PREH were similar in hypertensives and normotensives.

Gender influence on post-resistance exercise hypotension and hemodynamics.

Post-resistance exercise hypotension has been extensively described in men and women. However, gender influence on this response has not yet been clear. Gender might change post-exercise hemodynamics, since men and women respond differently during exercise. Thus, the purpose was to compare post-resistance exercise hypotension and its hemodynamic determinants in men and women. Normotensive subjects (22-male, 22-female) underwent 2 sessions: control (40 min of rest) and exercise (6 resistance exercises, 3 sets, 20 repetitions, at 40-50% of 1RM). Blood pressure, heart rate, and cardiac output were measured prior to and following interventions. Blood pressure decrease after exercise was similar between the genders. However, hemodynamic determinants responded differently in men and women. Systemic vascular resistance reduced in women (-4.6±1.9U, P<0.05), while cardiac output decreased in men (-0.6±0.2 L/min, P<0.05). This response was accompanied by a decrease in stroke volume in men (-21.6±5.1 ml, P<0.05) and a more pronounced increase in heart rate in men than in women (+11.3±1.3 vs. +6.5±1.7 bpm, P<0.05, respectively). In conclusion, post-resistance exercise hypotension was similar in men and women. However, its hemodynamic determinants differ between the genders, depending on cardiac output decrease in men and on systemic vascular resistance decrease in women.

Finger blood pressure during leg resistance exercise.

Blood pressure (BP) assessment during resistance exercise can be useful to avoid high BP, reducing cardiovascular risk, especially in hypertensive individuals. However, non-invasive accurate technique for this purpose is not available. The aim of this study was to compare finger photoplethysmographic (FPP) and intra-arterial BP values and responses during resistance exercise. Eight non-medicated hypertensive subjects (5 males, 30-60 years) were evaluated during pre-exercise resting period and during three sets of the knee extension exercise performed at 80% of 1RM until fatigue. BP was measured simultaneously by FPP and intra-arterial methods. Data are mean+/-SD. Systolic BP was significantly higher with FPP than with intra-arterial: at pre-exercise (157+/-13 vs. 152+/-10 mmHg; p<0.01) and the mean (202+/-29 vs. 198+/-26 mmHg; p<0.01), and the maximal (240+/-26 vs. 234+/-16 mmHg; p<0.05) values achieved during exercise. The increase in systolic BP during resistance exercise was similar between FPP and intra-arterial (+73+/-29 vs. +71+/-18 mmHg; p=0.59). Diastolic BP values and increases were lower with FPP. In conclusion, FPP provides similar values of BP increment during resistance exercise than intra-arterial method. However, it overestimates by 2.6+/-6.1% the maximal systolic BP achieved during this mode of exercise and underestimates by 8.8+/-5.8% the maximal diastolic BP.

Post-resistance exercise hypotension, hemodynamics, and heart rate variability: influence of exercise intensity.

UNLABELLED: The occurrence of post-exercise hypotension after resistance exercise is controversial, and its mechanisms are unknown. To evaluate the effect of different resistance exercise intensities on post-exercise blood pressure (BP), and hemodynamic and autonomic mechanisms, 17 normotensives underwent three experimental sessions: control (C-40 min of rest), low- (E40%-40% of 1 repetition maximum, RM), and high-intensity (E80%-80% of 1 RM) resistance exercises. Before and after interventions, BP, heart rate (HR), and cardiac output (CO) were measured. Autonomic regulation was evaluated by normalized low- (LF(R-R)nu) and high-frequency (HF(R-R)nu) components of the R-R variability. In comparison with pre-exercise, systolic BP decreased similarly in the E40% and E80% (-6 +/- 1 and -8 +/- 1 mmHg, P < 0.05). Diastolic BP decreased in the E40%, increased in the C, and did not change in the E80%. CO decreased similarly in all the sessions (-0.4 +/- 0.2 l/min, P < 0.05), while systemic vascular resistance (SVR) increased in the C, did not change in the E40%, and increased in the E80%. Stroke volume decreased, while HR increased after both exercises, and these changes were greater in the E80% (-11 +/- 2 vs. -17 +/- 2 ml/beat, and +17 +/- 2 vs. +21 +/- 2 bpm, P < 0.05). LF(R-R)nu increased, while ln HF(R-R)nu decreased in both exercise sessions. IN CONCLUSION: Low- and high-intensity resistance exercises cause systolic post-exercise hypotension; however, only low-intensity exercise decreases diastolic BP. BP fall is due to CO decrease that is not compensated by SVR increase. BP fall is accompanied by HR increase due to an increase in sympathetic modulation to the heart.

Previous exercise attenuates muscle sympathetic activity and increases blood flow during acute euglycemic hyperinsulinemia.

Insulin infusion causes muscle vasodilation, despite the increase in sympathetic nerve activity. In contrast, a single bout of exercise decreases sympathetic activity and increases muscle blood flow during the postexercise period. We tested the hypothesis that muscle sympathetic activity would be lower and muscle vasodilation would be higher during hyperinsulinemia performed after a single bout of dynamic exercise. Twenty-one healthy young men randomly underwent two hyperinsulinemic euglycemic clamps performed after 45 min of seated rest (control) or bicycle exercise (50% of peak oxygen uptake). Muscle sympathetic nerve activity (MSNA, microneurography), forearm blood flow (FBF, plethysmography), blood pressure (BP, oscillometric method), and heart rate (HR, ECG) were measured at baseline (90 min after exercise or seated rest) and during hyperinsulinemic euglycemic clamps. Baseline glucose and insulin concentrations were similar in the exercise and control sessions. Insulin sensitivity was unchanged by previous exercise. During the clamp, insulin levels increased similarly in both sessions. As expected, insulin infusion increased MSNA, FBF, BP, and HR in both sessions (23 +/- 1 vs. 36 +/- 2 bursts/min, 1.8 +/- 0.1 vs. 2.2 +/- 0.2 ml.min(-1).100 ml(-1), 89 +/- 2 vs. 92 +/- 2 mmHg, and 58 +/- 1 vs. 62 +/- 1 beats/min, respectively, P < 0.05). BP and HR were similar between sessions. However, MSNA was significantly lower (27 +/- 2 vs. 31 +/- 2 bursts/min), and FBF was significantly higher (2.2 +/- 0.2 vs. 1.8 +/- 0.1 ml.min(-1).100 ml(-1), P < 0.05) in the exercise session compared with the control session. In conclusion, in healthy men, a prolonged bout of dynamic exercise decreases MSNA and increases FBF. These effects persist during acute hyperinsulinemia performed after exercise.

Postexercise hypotension and hemodynamics: the role of exercise intensity.

AIM: Although postexercise hypotension (PEH) has already been extensively demonstrated, the influence of exercise intensity on its magnitude and mechanisms is still controversial. METHODS: Twenty-three normotensive subjects were submitted to a control (45 minutes of rest) and 3 exercise sessions (cycle ergometer, 45 minutes at 30%, 50% and 75% of .VO(2peak)) to investigate the role of exercise intensity on PEH. Blood pressure (BP - auscultatory), heart rate (HR - ECG), and cardiac output (CO - CO2 rebreathing) were measured before and after the control and exercise sessions. RESULTS: Systolic BP decreased significantly after exercise at 50% and 75% of .VO(2peak). Diastolic BP increased significantly during the control session, did not change after exercise at 30% of .VO(2peak), and decreased significantly after exercise at 50% and 75% of .VO(2peak). This fall was greater and longer after more intense exercise. CO and systemic vascular resistance (SVR) responses were similar between sessions, CO increased whereas SVR decreased significantly. Stroke volume (SV) increased and heart rate (HR) decreased following control and exercise at 30% of .VO(2peak) whereas SV decreased and HR increased after exercise at 50% and 75% of .VO(2peak). CONCLUSION: PEH is greater and longer after more intense exercise. BP profile is followed by a decrease in SVR and an increase in CO, what was not influenced by previous exercise. The increase in CO is caused by an increase in SV after rest and low intensity exercise and by an increase in HR after moderate and more intense aerobic exercise.

Salt supresses baseline muscle sympathetic nerve activity in salt-sensitive and salt-resistant hypertensives.

The objective of our study was to evaluate the role of the baroreflex control of peripheral sympathetic nervous system on the increase of muscle sympathetic nerve activity (MSNA) in salt-sensitive (SS) and salt-resistant (SR) hypertensives under low salt diet. In phase I mild-to-moderate hypertensive patients (n=5) received three diet periods: a first regular salt (RS1), a low salt (LS=20 meq Na+/day), followed by a second regular salt diet (RS2) with a 7-day duration of each. At the end of each period, sympathetic and heart rate baroreflex control were recorded. Baseline MSNA varied (P<0.005) from 18+/-8 (RS1) to 32+/-9 (LS) and to 14+/-9 (RS2) bursts per minute (bpm). In phase II additional patients (n=6) were included to have baseline MSNA, sympathetic and heart rate baroreflex control evaluated at the end of the LS and RS2. For all patients (n=11), there was a significant decrease of MSNA from 36+/-4 to 20+/-8 bpm on day 7 of LS to RS2 (P<0.05). The response of MSNA to a salt restriction was similar for SS and SR patients, who showed a change from 32+/-6 to 18+/-11 and from 36+/-9 to 17+/-7 bpm for SS and SR on day 7 of LS and RS2 diets, respectively (P<0.05). MSNA baroreflex gain was similar during phenylephrine infusions at day 7 of LS and RS2 (5.1+/-1.6 and 6.1+/-2.9 bpm/mmHg), but it was reduced under LS during sodium nitroprusside infusion (19.5+/-4.9 vs 8.9+/-0.7 bpm/mmHg) (P<0.05) for the whole group. Baroreflex control of MSNA was also similar during phenylephrine infusions under LS and RS2 diets for SS (4.0+/-0.9 and 3.3+/-0.2 bpm/mmHg) and for SR patients (10.1+/-2.5 and 5.6+/-1.5 bpm/mmHg). During nitroprusside infusion, baroreflex gain was significantly greater under RS2 for SR patients (19.5+/-2.6 bpm/mmHg) when compared to LS (11.2+/-5.2 bpm/mmHg) and the same significant difference was observed among SS patients (14.4+/-4.7 and 9.1+/-3.6 bpm/mmHg under RS2 and LS diets, respectively). There was no difference in heart rate baroreflex gain between LS and RS2 diets. Data support the hypotheses that (1) sodium supresses baseline MSNA in SS and SR hypertensives and (2) sodium restriction may impair baroreflex control of MSNA in SR and SS mild-to-moderate hypertensive patients during blood pressure reductions.

Mild chronic renal insufficiency induces sympathetic overactivity.

The objectives of this study were to evaluate baseline sympathetic nerve activity as well as the mechanisms of sympathetic overactivity in mild chronic renal insufficiency hypertension. Seven hypertensives with mild renal insufficiency, seven hypertensives with normal renal function and seven normotensives, age and weight-matched were studied on one session to evaluate baseline muscle sympathetic nerve activity measured in the peroneal nerve. The mild renal insufficiency hypertensives and the hypertensives with normal renal function were also studied to evaluate arterial baroreflex control of muscle sympathetic nerve activity assessed by increasing and decreasing blood pressure through continuous infusion of phenylephrine and sodium nitroprusside respectively. Baseline muscle sympathetic nerve activity was significantly higher in mild renal insufficiency hypertensives (34 bursts/min) when compared to hypertensives with normal renal function (24 bursts/min) and to normotensives (16 bursts/min). Baroreflex control of muscle sympathetic nerve activity was (in absolute values) 15.2 in hypertensives with normal renal function vs 2.6 in mild renal insufficiency hypertensives (P < 0.05) during phenylephrine and 6.3 vs 8.2 during nitroprusside infusions. Mild renal insufficiency hypertensives showed sympathetic overactivity when compared to hypertensives with normal renal function and to normotensives. This finding demonstrates that elevated sympathetic activity may be precociously detected in renal insufficiency. Baroreflex gain to phenylephrine was blunted in mild renal insufficiency hypertensives when compared to hypertensives with normal renal function, suggesting that bradycardic response in mild renal insufficiency is blunted.

Muscle metaboreflex control is diminished in normotensive obese women.

There is no information about the muscle metaboreflex control in obese individuals. In 40 normotensive obese women (OW; body mass index 33.5 +/- 0.4 kg/m2, age 32.4 +/- 1.1 yr) and 15 age-matched, normotensive lean women (LW; body mass index 22.7 +/- 0.8 kg/m2, age 34.4 +/- 1.4 yr), we measured muscle sympathetic nerve activity (MSNA) and forearm blood flow (FBF) in the nonexercising forearm during static exercise at 10 and 30% of maximal voluntary contraction (MVC). Baseline MSNA (38 +/- 2 vs. 31 +/- 1 bursts/min, P = 0.001) and mean blood pressure were significantly higher in OW compared with LW. FBF was significantly lower, whereas forearm vascular resistance was significantly higher in OW. During 10% MVC, MSNA increased similarly in both groups, but during 30% MVC, MSNA was higher in LW. FBF and forearm vascular resistance responses during both 10 and 30% MVC were similar between groups. During posthandgrip circulatory arrest, MSNA remained significantly elevated compared with baseline in both groups, but this increase was significantly lower in OW (3.8 +/- 0.82 vs. 9.4 +/- 1.03 bursts/min, P = 0.002). In conclusion, muscle metaboreflex control of MSNA is blunted in OW. MSNA responses are not augmented during selective activation of central command/mechanoreceptors and metaboreceptors, despite increased MSNA levels in OW. Muscle vasodilatory response during graded handgrip isometric exercise is preserved in OW.

Abnormal neurovascular control during exercise is linked to heart failure severity.

The purpose of this study was to determine if abnormalities of sympathetic neural and vascular control are present in mild and/or severe heart failure (HF) and to determine the underlying afferent mechanisms. Patients with severe HF, mild HF, and age-matched controls were studied. Muscle sympathetic nerve activity (MSNA) and forearm vascular resistance (FVR) in the nonexercising arm were measured during mild and moderate static handgrip. MSNA during moderate handgrip was higher at baseline and throughout exercise in severe HF vs. mild HF (peak MSNA 67 +/- 3 vs. 54 +/- 3 bursts/min, P < 0.0001) and higher in mild HF vs. controls (33 +/- 3 bursts/min, P < 0.0001), but the change in MSNA was not different between the groups. The change in FVR was not significantly different between the three groups during static exercise. During isolation of muscle metaboreceptors, MSNA and blood pressure remained elevated in normal controls and mild HF but not in severe HF. During mild handgrip, the increase in MSNA was exaggerated in severe HF vs. controls and mild HF, in whom MSNA did not increase. In summary, the increase in MSNA during static exercise in severe HF appears to be attributable to exaggerated central command or muscle mechanoreceptor control, not muscle metaboreceptor control.

Factors affecting post-exercise hypotension in normotensive and hypertensive humans.

BACKGROUND: Post-exercise hypotension has been extensively described under laboratory conditions. However, studies investigating the persistence of this post-exercise decrease in blood pressure for longer periods have produced controversial results. The present investigation was conducted to verify the effect of a single bout of exercise on ambulatory blood pressure and to identify potential factors that might influence this post-exercise ambulatory blood pressure fall. DESIGN: The study was a randomized controlled clinical trial. METHODS: Thirty normotensive and 23 hypertensive subjects were submitted to two ambulatory blood pressure monitorings (using the SpaceLabs 90207, SpaceLabs, Redmond, Washington, USA), which were performed after 45min of seated rest (control session) or cycling exercise at 50% peak oxygen uptake (exercise session). RESULTS: Normotensive subjects demonstrated a lower 24h blood pressure level in the exercise session. Hypertensive patients showed no significant difference in ambulatory blood pressure level between the two experimental sessions. Further data analysis revealed that approximately 65% of the subjects in both groups experienced a fall in blood pressure after exercise. Moreover, in the normotensive subjects, this blood pressure fall was significantly and positively correlated with clinic and ambulatory blood pressure, and negatively correlated with weight and body mass index. The blood pressure response to exercise was also greater in women. In the hypertensive patients, the post-exercise blood pressure decrease was significantly and positively correlated with clinic and ambulatory blood pressure as well as with the peak oxygen uptake, and negatively correlated with age and body mass index. CONCLUSIONS: The post-exercise ambulatory blood pressure fall observed in normotensive and hypertensive humans depends on individual characteristics. Moreover, in both normotensive and hypertensive humans, post-exercise ambulatory hypotension is greater in subjects with a higher initial blood pressure level.

Postexercise responses of muscle sympathetic nerve activity and blood flow to hyperinsulinemia in humans.

Although insulin and exercise cause dramatic changes in physiological parameters, the impact of exercise on neural and hemodynamic responses to insulin administration has not been described. In a study of the effects of a single bout of exercise on blood pressure (BP), muscle sympathetic nerve activity (MSNA), and forearm blood flow (FBF) responses to insulin infusion during the postexercise period, 11 healthy men underwent, in a random order, two hyperinsulinemic euglycemic clamps performed after 45 min of 1) bicycle exercise (50% peak O(2) uptake, Exercise session) and 2) seated rest (Control session). Data were analyzed during baseline and steady-state periods. Although insulin levels and insulin sensitivity were similar, baseline plasma glucose levels were significantly lower in the Exercise than in the Control session. Mean BP was significantly lower (3%) and FBF was higher (27%) in the Exercise session. Exercise increased insulin-induced MSNA enhancement (84%) without changing FBF and BP responses to hyperinsulinemia. In conclusion, a single bout of exercise that does not alter insulin sensitivity exacerbates insulin-induced increase in MSNA without changing FBF and BP responses to hyperinsulinemia.

Baroreflex control of muscle sympathetic nerve activity in mild hypertension.

The importance of the arterial baroreflex control of muscle sympathetic nerve activity (MSNA) has been investigated in physiological conditions and in cardiovascular dysfunctions. However, there is no consensus about the role played by the MSNA in hypertensive states, probably due to the diversity of the methods used to study the arterial baroreflex control of MSNA. In the present study we evaluated the reflex changes in MSNA by increasing and decreasing the mean arterial pressure (MAP) through 1 min intravenous infusion of phenylephrine (1 microgram/kg) and sodium nitroprusside (1 microgram/kg), respectively, in eight normotensive and eight mild hypertensive subjects. Both MAP and MSNA were significantly higher in hypertensive (117 +/- 2 mm Hg and 30 +/- 3 bursts/min) than in normotensive (96 +/- 4 mm Hg and 20 +/- 3 bursts/min) subjects. The reflex gain was calculated by the ratio percent of changes in MSNA/percent changes in MAP. The maximal reflex gain was statistically similar in normotensive and hypertensive groups during phenylephrine (5.1 +/- .4 v 4.3 +/- 0.4 bursts/mm Hg, respectively) and nitroprusside (10.7 +/- 2.3 v 8.1 +/- 1.3 bursts/mm Hg, respectively) infusion. The present data showing that arterial baroreflex control of MSNA is not depressed in hypertensive subjects indicate that the elevated basal MSNA and the mild hypertension in human beings is not a consequence of baroreflex control of MSNA dysfunction.

Microneurografia: técnica para estudo da regulaçäo cardiovascular pelo sistema nervoso simpático em humanos / Microneurography: technique to study cardiovascular regulation through the sympathetic nervous system in humans

A microneurografia é um método eficaz e seguro para o registro intraneural direto da atividade nervosa simpática para o músculo e para pele em humanos. A técnica e suas aplicaçöes para o estudo da funçäo autonômica seräo discutidos neste artigo. Será abordada a regulaçäo da atividade nervosa simpática em diferentes situaçöes clínicas e/ou estímulos, tais como hipertensäo arterial essencial, hipertensäo experimental por mineralocorticóide, exercício, estresse mental, teste do gelo, hiperinsulinemia e ingestäo oral de álcool

[Microneurography: technique to study cardiovascular regulation by the sympathetic nervous system in humans]. / Microneurografia: técnica para estudo da regulação cardiovascular pelo sistema nervoso simpático em humanos.

Microneurography is a valuable and safe method for direct intraneural recording of sympathetic nerve activity to muscle and skin in humans. The technique and its application for the study of autonomic function will be briefly discussed. The regulation of muscle sympathetic nerve activity will be focused in different clinical situations and or stimuli, such as: essential hypertension, mineralocorticoid induced hypertension, exercise mental arithmetic stress, cold pressor test, hyperinsulinemia, oral alcohol ingestion.

[Comparative and double-blind study of the efficacy and safety of cilazapril compared to nifedipine retard in the treatment of mild and moderate arterial hypertension]. / Estudo comparativo duplo-cego da eficácia e segurança do cilazapril comparadas à nifedipina "retard" no tratamento da hipertensão arterial leve e moderada.

PURPOSE: To evaluate the antihypertensive efficacy and safety of cilazapril compared to nifedipine retard in mild to moderate hypertension. METHODS: forty randomized out-patients with mild moderate hypertension, diastolic pressure (DP) between 95 and 115 mmHg, with placebo for 15 days were randomized and allocated for treatment, double-blind, once daily with cilazapril 2.5 mg (n = 20) or nifedipine retard 20 mg (20 = n) for four weeks. The non-responders (DP > 90mmHg) had the dosage increased twice, b.i.d., while responders were maintained up to 10 weeks. Clinical visits were performed before, at baseline and every two weeks and the laboratory test was performed after placebo run-in, 4th and 10th weeks of treatment. RESULTS: The blood pressure (BP) were similar between groups at the end of the placebo (cilazapril 151 +/- 14/103 +/- 5 - nifedipine 157 +/- 17/108 +/- 7mmHg, p > 0.05). DP decreased already at second weeks (cilazapril 95 +/- 9 - nifedipine 96 +/- 11mmHg, p < 0.05, compared to week 0) in both groups at the end of study with no difference inter groups. BP normalization was obtained in 58% of the patients with cilazapril and in 61% in the nifedipine group. Adverse biochemical effects were not observed in any group. Six (16%) patients of the cilazapril and 15 (39%) of nifedipine related collateral events, although no difference were observed between groups. CONCLUSION: Cilazapril 2.5 to 25mg normalized BP in 58% of mild and moderate hypertension patients, and this efficacy was similar to sustained-release nifedipine 20 to 40mg. Cilazapril had no adverse effects on the biochemical parameters with low incidence of collateral effects.