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Using ion-exchange chromatography of dialyzed human urine from healthy and hypertensive patients, we detected two peaks of angiotensin I-converting enzyme (ACE) activity on hippuryl-His-Leu eluted at ionic strengths of 0.7 (F1 peak) and 1.25 (F2 peak) mS. These hydrolytic activities decreased gradually in the urine of patients submitted to isradipine treatment, F2 and F1 disappearing after 12 and 24 hours, respectively. By Western blot analysis, the urine fractions corresponding to both peaks from healthy and untreated patients presenting ACE activity and from treated patients (24 hours) without this activity were recognized by an ACE-specific antibody. These results indicated that ACE was present but inhibited in the urine of isradipine-treated patients. In vitro assays with ACE isolated from human urine and guinea pig plasma demonstrated that the enzyme is inhibited by isradipine and other commercially available calcium channel blockers, such as felodipine, nifedipine, and verapamil. A noncompetitive inhibition was observed with all calcium channel blockers studied. In conclusion, these results suggest that besides the primary effect on calcium channels, the more commonly used calcium channel blockers are also ACE inhibitors. The development of efficient calcium channel blockers with higher ACE inhibitory activity could result in interesting bifunctional antihypertensive drugs.

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Atherosclerosis is considered an important cause of morbidity and mortality in systemic lupus erythematosus (SLE). Endothelial dysfunction represents an important factor in the onset of atherosclerosis. Objective'. To assess endothelial function and the risk factors for atherosclerosis in adolescents with SLE. Subjects: Thirty-five adolescents with SLE aged between 10-18 years and 27 age-and sex-matched controls. Methods: Endothelial function was assessed using a high-resolution ultrasound device (Philips ATL, HDI-3000 model) with a linear array transducer (4.0-7.0 MHz). Measures of diameter and flow were performed at rest, during reactive hyperemia and after glyceryl trinitrate. Total cholesterol and fractions, triglycerides, creatinine, fasting glucose, anticardiolipin antibodies, lupus anticoagulant and plasma homocysteine, as well as, cumulative oral corticoid dose were considered in order to establish the risk factors for atherosclerosis. Results: No significant difference was found between the two groups regarding endothelial function. Although dilation at 90" after cuff deflation had been smaller in patients than in controls, the difference was not statistically significant. Patients had higher levels of total cholesterol (p=0.02), VLDL (p=0.01), triglycerides (p=0.01), and homocysteine (p<.001) compared with controls. Sixty eight percent of our patients showed hyperhomocysteinemia, yet, we did not find any correlation between these values and flowmediated dilation. Conclusion: According to our results, adolescents with SLE do not present alterations in endothelial function as assessed by ultrasound. However, these patients did demonstrate risk factors such as dyslipidemia and hyperhomocysteinemia for the development of atherosclerosis.

Purpose -To evaluate left ventricular mass (LVM) index in hypertensive and normotensive obese individuals. Methods -Echocardiographic evaluation of hypertensive individuals is based on preestablished guidelines for detecting left ventricular hypertrophy, determined in relation to populations of normotensive individuals. In turn, the definition of normal left ventricular mass implies its correction by influencing physiological factors. Thus, sex, body habitus, and possibly age are of importance in this correction.The best index of left ventricular mass is that obtained using the physiological scale of weight and height variables, regarding both men and women.Therefore, the ideal index would be lean body mass 1 , but this method is not practical and has not been used. Thus, indexing ventricular mass by body surface area (BSA) is preferred 2 . However, such an index leads to underestimation of left ventricular hypertrophy in obese individuals (with a greater BSA), because its regards obesity as a continuous physiological variable that would determine increases in left ventricular mass also on a physiological scale 3 . To correct this, use of mass by height, whose limits are within the physiological range and thus maintain a normal and not a pathological relation to ventricular mass, has been proposed as an index [4][5][6] . More recent studies 7-11 further suggest that left ventricular mass index should be determined by height or even height raised to a power of 2, 2.7, or 2.13, because no first order relation has been demonstrated between height and left ventricular mass.In this sense, some selection criteria have been established that have been used for the correction of mass by these proposed indexers (men -126/143g/m; 49.2g/m 2.7 ; women -105/102g/m; 46.7g/m 2.7 )4,11 . Such criteria, up to the present, have preferentially been used in larger population studies 11,[13][14][15][16] with the purpose of detecting the impact of the different indexes used on the prevalence of

The aim of this study was to analyze the thickness of the intima-media complex (IMC) using a noninvasive method. The carotid and femoral common arteries were evaluated by noninvasive B-mode ultrasound in 63 normotensive and in 52 hypertensive subjects and the thickness of the IMC was tested for correlation with blood pressure, cardiac structures and several clinical and biological parameters. The IMC was thicker in hypertensive than in normotensive subjects (0.67 ± 0.13 and 0.62 ± 0.16 vs 0.54 ± 0.09 and 0.52 ± 0.11 mm, respectively, P<0.0001). In normotensive patients, the simple linear regression showed significant correlations between IMC and age, body mass index and 24-h systolic blood pressure for both the carotid and femoral arteries. In hypertensives the carotid IMC was correlated with age and 24-h systolic blood pressure while femoral IMC was correlated only with 24-h diastolic blood pressure. Forward stepwise regression showed that age, body mass index and 24-h systolic blood pressure influenced the carotid IMC relationship (r 2 = 0.39) in normotensives. On the other hand, the femoral IMC relationship was influenced by 24-h systolic blood pressure and age (r 2 = 0.40). In hypertensives, age and 24-h systolic blood pressure were the most important determinants of carotid IMC (r 2 = 0.37), while femoral IMC was influenced only by 24-h diastolic blood pressure (r 2 = 0.10). There was an association between carotid IMC and echocardiographic findings in normotensives, while in hypertensives only the left posterior wall and interventricular septum were associated with femoral IMC. We conclude that age and blood pressure influence the intima-media thickness, while echocardiographic changes are associated with the IMC.