1. Aldosterone has been considered a key hormone in the regulation of water, sodium and potassium metabolism, thus influencing blood pressure regulation. More recently, several studies have demonstrated that aldosterone is also produced in extra-adrenal tissues (e.g. the heart), suggesting a paracrine effect for aldosterone, such as to increase collagen synthesis in the heart. 2. Because aldosterone production in the heart increases after myocardial infarction (MI), we investigated the effect of chronic administration of spironolactone, an aldosterone receptor antagonist, in rats after MI compared with the effects produced by losartan and hydralazine. 3. Myocardial infarction was produced in male Wistar rats by surgical ligature of the left coronary artery. Sham-operated animals were used as controls. 4. Spironolactone (20 mg/kg per day), losartan (15 mg/kg per day) or hydralazine (20 microg/kg per day) were administered after MI and used for 1 month. 5. At the end of the treatment period, animals underwent haemodynamic recording (arterial and intraventricular pressures). The collagen content of the heart was evaluated by measuring the hydroxyproline (OH-Pro) concentration in right (RV) and left ventricle (LV) muscle fragments. 6. Infarct size was unaffected by drug treatments. The increased LV end-diastolic pressure observed in MI rats was prevented by losartan and remained unchanged following administration of spironolactone or hydralazine. 7. Losartan prevented RV and LV hypertrophy, as well as collagen proliferation in both ventricles, after MI. The postinfarction hypertrophy observed in RV and LV after MI remained unchanged in infarcted groups treated with spironolactone or hydralazine. 8. The OH-Pro concentration was significantly reduced in LV muscle in the MI group treated with spironolactone (682 +/- 40 vs 557 +/- 21 microg/g for MI vs MI + spironolactone, respectively; P < 0.05), an effect not observed in the hydralazine-treated group. 9. These data suggest that spironolactone prevents collagen proliferation in the surviving myocardium by mechanisms independent of the loading conditions of the heart chambers. Control of postinfarction hypertrophy and collagen accumulation produced by losartan seems to depend on the reduction in loading conditions of the heart chambers.

Purpose -To determine angiotensin converting enzyme (ACE) activity in the heart of infarcted rats and to investigate the effects of captopril and losartan on the post-infarction remodeling process. Methods -Myocardial infarction (MI) was produced in Wistar rats Métodos -O IM foi produzido em ratos Wistar por ligadura de ramos da artéria coronária esquerda. Os controles (Con) foram submetidos a uma cirurgia fictícia. Animais com IM e Con foram tratados com captopril (30mg/kg/dia) ou losartan (15mg/kg/dia) e estudados 30 dias após, determinando-se a atividade da ECA nos ventrí-culos direito (VD) e esquerdo (VE), as alterações hemodinâmicas e as concentrações de hidroxiprolina (OH-Pro) e proteína total no VD e VE.Resultados Ativação da Enzima Conversora de Angiotensina no Coração após Infarto do Miocárdio e suas Repercussões no RemodelamentoVentricular Artigo OriginalA importância do sistema renina-angiotensina-aldosterona (SRAA) na regulação a longo prazo do volume extracelular, do balanço dos íons Na e K da pressão arterial (PA) tem sido reconhecida há muito tempo. O grau de ativação da alça endócrina desse sistema reside principalmente no

Introduction: The present study investigated cancer prevalence and associated factors among HIV-infected individuals attending an AIDS outpatient clinic in Vitória, State of Espírito Santo, Brazil. Methods: A sectional study was conducted among HIV infected adults attending an AIDS outpatient clinic in Vitória, State of Espírito Santo, Brazil. Demographic, epidemiological and clinical data were abstracted from medical records, including cancer diagnoses; nadir and current CD4 cell count, HIV viral load, time on antiretroviral treatment (ART), type of ART and smoking status. Results: A total of 730 (91.3%) patients were included in the study. Median age was 44.0 [interquartile range (IQR): 35–50.3] years; median time since HIV diagnosis was 5.5 years (IQR: 2–10); 60% were male; and 59% were white. Thirty (4.1%) cases of cancer were identified of which 16 (53%) were AIDS defining cancers and 14 (47%) were non-AIDS defining malignancies. Patients diagnosed with cancer presented higher chance of being tobacco users [OR 2.2 (95% CI: 1.04–6.24)]; having nadir CD4 ≤200 cells/mm3 [OR 3.0 (95% CI: 1.19–7.81)] and higher lethality [OR 13,3 (95% CI: 4,57–38,72)]. Conclusions: These results corroborate the importance of screening for and prevention of non-AIDS defining cancers focus in HIV-infected population, as these cancers presented with similar frequency as AIDS defining cancers.

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