Association of urinary 90 kDa angiotensin- converting enzyme with family history of hypertension and endothelial function in normotensive individuals

We described angiotensin-I-converting enzyme (ACE) isoforms with molecular masses of 190, 90, and 65 kDa in the urine of normotensive offspring of hypertensive subjects. Since they did not appear in equal amounts, we suggested that 90 kDa ACE might be a marker for hypertension. We evaluated the endothelial response in normotensive offspring with or without family history of hypertension and its association with the 90 kDa ACE in urine. Thirty-five normotensive subjects with a known family history of hypertension and 20 subjects without a family history of hypertension, matched for age, sex, body weight, and blood pressure, were included in the study. Endothelial function was assessed by ultrasound and a sample of urine was collected for determination of ACE isoforms. In the presence of a family history of hypertension and detection of 90 kDa ACE, we noted a maximal flow mediated dilation of 12.1 ± 5.0 vs 16.1 ± 6.0 percent in those without a previous history of hypertension and lacking urinary 90 kDa ACE (P < 0.05). In subjects with a family history of hypertension and presenting 90 kDa ACE, there were lower levels of HDL-cholesterol (P < 0.05) and higher levels of triglycerides (P < 0.05). Subjects with 90 kDa ACE irrespective of hypertensive history presented a trend for higher levels of triglycerides and HDL-cholesterol (P = 0.06) compared to subjects without 90 kDa ACE. Our data suggest that the 90 kDa ACE may be a marker for hypertension which may be related to the development of early atherosclerotic changes.

Stress and hypertension: studies in three experimental models

The effects of three models of stress upon blood pressure and central responsiveness to angiotensin II (AII) and noradrenaline (NA) were assessed in rats. Considering general parameters of stress efficacy, all models were effective to induce stress but hypertension only occurred in animals submitted to rapid eye movement sleep deprivation (REM-sd) and electric shock (ES). An increased central pressor effect of AII and NA was observed in these groups. On the other hand, restriction (R) did not increase blood pressure or central responsiveness to AII or NA. Instead of hypertension, R induced gastric ulcers and testis atrophy. Thus, hypertension occurs only in some models of stress and may be due to increased central responsiveness to AII and NA.

Microalbuminuria, arterial blood pressure and retinopathy in insulin dependent diabetes

In order to evaluate the relationship between urinary albumin excretion, arterial blood pressure and diabetic retinopathy in insulin dependent diabetics we examined 55 patients without clinical proteinuria and whose disease had started before the age of 30. Each patient was asked to collect at least one overnight timed urine sample for albumin analysis by an ELISA method. Normoalbuminuria was defined as urinary albumin excretion (UAE) of < 20 mug/min (n = 32) and microalbuminuria as 21-200 mug/min (n = 23). Patients with microalbuminuria showed higher levels of blood pressure, serum creatinine and glicosylated haemoglobin as compared to normoalbuminuric patients. Significant correlation was observed between diastolic blood pressure and UAE (r = 0.52; p < O.001).Preproliferative and proliferative diabetic retinopathy was detected in 9 patients (l6.4 per cent). All of them had diabetes for more than 10 years, elevated UAE and diastolic blood pressure equal or higher than 85 mmHg. In our population of insulin dependent diabetics we found a high prevalence of microalbuminuria which is considered to be predictive of the latter development of diabetic nephropathy. Microalbuminuria is associated with elevated blood pressure and diabetic retinal lesions. We conclude that urinary albumin excretion should be monitored in patients with insulin dependent diabetes to detect those who should be considered at risk of developing nephropathy and retinopathy.

Tratamento da crise hipertensiva com captopril. / Treatment of hypertensive crisis with captopril

Avaliou-se a eficiencia do captopril, um inibidor da enzima conversora, no tratamento de 28 pacientes em crise hipertensiva de variadas etiologias: 12 com hipertensao arterial maligna, 6 com hipertensao acelerada, 4 com hipertensao renovascular e 6 com hipertensao renovascular arterial refrataria. A resposta imediata ao captopril foi mais intensa nos pacientes portadores de hipertensao arterial acelerada e maligna e hipertensao renovascular. Assim, em 14 dos 18 pacientes com hipertensao acelerada e maligna, doses entre 150 e 300 mg de captopril foram suficientes para reduzir a pressao arterial a niveis proximos da normalidade. Nos outros 4 pacientes deste grupo, necessitou-se de um diuretico para controlar a pressao arterial. Os 4 pacientes com hipertensao renovascular apresentaram reducoes similares na pressao arterial, porem com doses menores de captopril. Os 6 pacientes portadores de hipertensao arterial refrataria apresentaram menores reducoes pressoricas com doses de captopril entre 50 e 150 mg.Concluiu-se que captopril foi eficaz para o tratamento inicial de crises hipertensivas de diversas etiologias