Angiotensin converting enzyme gene polymorphism and carotid atherosclerosis in a low-risk population.

OBJECTIVES: Angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphism has been shown to be an independent risk factor for myocardial infarction and other cardiovascular diseases. The aim of the study was to investigate the relationship between ACE genotype and carotid atherosclerosis evaluated by ultrasonography. PATIENTS AND METHODS: ACE I/D polymorphism was determined in 240 low-risk patients (mean age 53.6 +/- 7 years) in relation to traditional risk factors and the degree of carotid atherosclerosis. Intimal-medial thickness was measured at the level of the common carotid artery, bifurcation and internal carotid on both sides. Patients were defined as normal (n = 47, intimal-medial thickness <1.0 mm), thickened (n = 56, intimal-medial thickness > or = 1.0 and < or = 1.3 mm in the thickest wall) or with an atherosclerotic plaque (n = 137, intimal-medial thickness >1.3 mm for at least one level of examination). Age, sex, body mass index, blood pressure levels and prevalence of other risk factors were similar in the three groups. I/D polymorphism was determined by polymerase chain reaction using specific primers and genomic DNA from leukocytes as template. Plasma ACE levels, plasma renin activity and plasma aldosterone were evaluated in all patients by standard procedures. RESULTS: No significant differences were found in humoral parameters, ACE, genotype distribution and the corresponding allele frequency among the three groups of patients. Only ACE plasma levels were significantly higher in the DD and ID genotypes compared with the II genotype (DD 14.27 +/- 5.05 IU/ml, ID 12.70 +/- 4.31 IU/ml; II 8.04 +/- 3.45 IU/ml). The mean intimal-medial thickness was similar in all three genotypes. CONCLUSION: Although ACE genotype has been shown to be related to coronary atherosclerosis, the present data do not indicate that the DD genotype is associated with carotid atherosclerosis. However, further studies of larger populations are needed to clarify whether genetic ACE polymorphism is associated with carotid atherosclerosis.

Urinary kallikrein excretion and blood pressure response to angiotensin converting enzyme inhibitors and calcium antagonists in hypertensive patients.

OBJECTIVE: To investigate whether the hypotensive effects of angiotensin converting enzyme (ACE) inhibitors in comparison with those of calcium antagonist might be predicted by urinary kallikrein activity, a marker of the activity of the renal kallikrein-kinin system. DESIGN: Seventy-five essential hypertensive patients were randomly assigned to treatment with ACE inhibitors (enalapril or lisinopril 20 mg once a day) or with calcium antagonists (nifedipine 20 mg twice a day or lacidipine 4 mg once a day). Fifty-four had normal (NK) and 21 low (LK) kallikrein activity. Blood pressure was measured after 2 weeks, and 3 and 6 months. Patients whose diagnostic blood pressure, 2 weeks after the first dose, decreased by at least 15 mmHg or was < or = 90 mmHg were defined as responders. The others were defined as non-responders. In non-responders a second drug was added and the patients were not considered for further analysis. METHODS: Urinary kallikrein activity was determined by a spectrophotometric assay using a synthetic chromogenic substrate. RESULTS: After 2 weeks therapy with ACE inhibitors 88% of NK patients were responders, whereas in the LK subgroup 40% were responders, a significant difference between subgroups. For the patients treated with calcium antagonists, conversely, 59% of NK patients were responders in comparison with 82% of the LK subgroup, a significant difference between drug groups. After 3 and 6 months of treatment blood pressure was significantly lower in NK patients treated with ACE inhibitors and in LK patients treated with calcium antagonists. In the NK group on ACE inhibitors the mean arterial pressure after the first dose was significantly related to that observed after 6 months (n = 0.71, P < 0.01). CONCLUSIONS: Our data indicate that urinary kallikrein activity may represent an index to predict the chronic antihypertensive effect not only of ACE inhibition but also of calcium antagonism, and support the concept that the renal kallikrein-kinin system might play some contributory role in modulating the hypotensive action of ACE inhibitors.

[Evaluation of intra-erythrocyte Na+ activity in persons at high risk for essential arterial hypertension and as an aid in differential diagnosis from secondary forms of hypertension]. / Valutazione della "Na+ activity" intra-eritrocitaria nei soggetti a rischio di ipertensione arteriosa essenziale e come ausilio nella diagnostica differenziale con le forme di ipertensione secondaria.

The intracellular "Na+ activity" was measured in erythrocytes of normotensive subjects (46), in essential hypertensive patients (18), in their children (20) and in patients with secondary hypertension (8). In normotensive subjects without a genetic trait of hypertension intracellular "Na+ activity" was 7.3 +/- 0.8 mmol/l, in secondary hypertensive patients was 7.5 +/- 0.6 mmol/l, in essential hypertensive patients was 10.9 +/- 1.1 mmol/l and in their children was 8.6 +/- 2.1 mmol/l. In this group (children) it was possible to differentiate between 2 population, the 1 degree with height intracellular "Na+ activity" (8); the 2 degrees with normal intracellular "Na+ activity".

[HbAlc in diabetic subjects in progressive deterioration of the metabolic situation]. / HbAlc in soggetti diabetici in progressivo peggioramento della stuazione metabolica.

Five subjects with type I and type II diabetes mellitus under worsening diabetic control were studied and their HbAlc levels were monitored over three months. There was a strong rise of HbAlc paralleling plasma glucose, while serum cholesterol and triglyceride levels do not rise significantly. These findings confirm that the glycosylation of haemoglobin in vivo reflects the mean blood glucose levels over the previous few weeks and suggest that the trouble of lipid metabolism in diabetes is a slower and more indirect expression of the derangement in diabetic control than HbAlc.

[Dexamethasone and its role in the prolactin secretion after TRH]. / Dexamethasone and its role in the prolactin secretion after TRH.

In 5 normal women plasma prolactin concentration after microg. 200 of TRH has been evaluated under treatment with mg 0.75/6h for three days of dexamethasone. No difference has been observed as regards to subjects without dexamethasone. The data suggest that the inhibition of adrenal cortex glucocorticoid and androgen hormones doesn't influence prolactin concentration after TRH.