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Cerebrovascular Diseases (CVD) comprise a wide spectrum of disorders, all sharing an acquired or inherited alteration of the cerebral vasculature. CVD have been associated with important changes in systemic and tissue Renin-Angiotensin System (RAS). The aim of this review was to summarize and to discuss recent findings related to the modulation of RAS components in CVD. The role of RAS axes is more extensively studied in experimentally induced stroke. By means of AT1 receptors in the brain, Ang II hampers cerebral blood flow and causes tissue ischemia, inflammation, oxidative stress, cell damage and apoptosis. On the other hand, Ang-(1-7) by stimulating Mas receptor promotes angiogenesis in brain tissue, decreases oxidative stress, neuroinflammation, and improves cognition, cerebral blood flow, neuronal survival, learning and memory. In regard to clinical studies, treatment with Angiotensin Converting Enzyme (ACE) inhibitors and AT1 receptor antagonists exerts preventive and therapeutic effects on stroke. Besides stroke, studies support a similar role of RAS molecules also in traumatic brain injury and cerebral aneurysm. The literature supports a beneficial role for the alternative RAS axis in CVD. Further studies are necessary to investigate the therapeutic potential of ACE2 activators and/or Mas receptor agonists in patients with CVD.

As doencas inflamatorias intestinais (DIIs) sao desordens cronicas de etiopatogenia nao esclarecida, cuja incidencia tem aumentado globalmente. Evidencias apontam que a suscetibilidade genetica associada a fatores ambientais sao capazes de determinar resposta imune anormal e comprometimento da barreira epitelial do intestino. Inumeras pesquisas demonstram uma possivel conexao fisiopatologica das DIIs com a microbiota intestinal (MI), sobretudo em casos da alteracao de sua composicao - disbiose. Embora controversa, a continuidade da investigacao nesta area faz-se necessaria para elucidar tal relacao. OBJETIVOS: Apresentar uma revisao sobre a correlacao entre as DIIs e MI, vislumbrando um possivel papel da disbiose na etiopatogenia dessas doencas e avaliar a aplicabilidade prognostica e terapeutica dos resultados encontrados. METODOLOGIA DE BUSCA: Utilizou-se pesquisa na plataforma PubMed de revisoes literarias com os termos “Inflammatory Bowel Disease”, “Microbiome” e “Microbiota” com os pesquisadores booleanos AND e OR respectivamente entre os termos. DISCUSSAO: A principal hipotese acerca da patogenia das DIIs consiste na interacao da MI com fatores extrinsecos, causando uma quebra ou penetracao da barreira epitelial das celulas intestinais, internalizando antigenos nas camadas submucosas. Em individuos geneticamente suscetiveis, uma resposta imune aberrante contra a MI invasora e desencadeada, gerando a inflamacao intestinal. A respeito de sua constituicao, constatou-se que alguns grupos de bacterias interferem no desenvolvimento das DIIs e em seu grau de complicacoes, principalmente relacionados a uma reducao da diversidade da MI. Tendo em vista este cenario, propostas terapeuticas visam a correcao da MI para o tratamento das DIIs. CONSIDERACOES FINAIS: Conhecer o papel da MI nas DII e de extrema importância para seu entendimento fisiopatologico. Futuramente, esclarecer como essa associacao ocorre podera permitir, atraves da manipulacao da MI, o desenvolvimento de novos alvos terapeuticos e a identificacao precoce dos pacientes de risco alem de prever fenotipos, evolucoes e possiveis complicacoes das doencas.

Despite the current availability of safe and efficient drugs for treating hypertension, a substantial number of patients are drug-resistant hypertensives. Aiming this condition, a relatively new approach named catheter-based renal denervation was developed. We have now a clinically relevant time window to review the efficacy of renal denervation for treating this form of hypertension. This short review addresses the physiological contribution of renal sympathetic nerves for blood pressure control and discusses the pros and cons of renal denervation procedure for the treatment of resistant hypertension. Resumo Em que pese a atual disponibilidade de medicamentos seguros e eficientes para o tratamento da hipertensão, um número significativo de pacientes sofre de hipertensão arterial resistente a tratamento medicamentoso. Em vista dessa condição, foi desenvolvida uma abordagem relativamente nova, denominada denervação renal por cateter. Dispomos atualmente de uma janela de tempo clinicamente relevante para analisar a eficácia da denervação renal no tratamento dessa modalidade de hipertensão. A presente revisão aborda a contribuição fisiológica dos nervos renais simpáticos no controle da pressão arterial e discute os prós e contras do procedimento de denervação renal no tratamento da hipertensão resistente.

Chagas disease (CD) is an important cause of cardiomyopathy in South America. The pathophysiology of CD is still a matter of debate. Renin Angiotensin System (RAS) components are clearly involved in cardiovascular diseases. RAS molecules interact with nitric oxide (NO) pathway in blood vessel and heart tissue. Thus, the aim of this study is to investigate possible changes in RAS molecules during the infection with Y strain T. cruzi and in response to acute administration of an inhibitor of the enzyme NO synthase, l -NAME. Male Holtzman rats were inoculated intraperitoneally with Y strain T. cruzi and received l -NAME or tap water from one day before the infection until 13 or 17 days post infection (dpi). Angiotensin converting enzyme 1 (ACE1) levels were significantly higher at day 17 when compared to baseline in atrium, whereas, in ventricle, ACE2 levels were significantly higher in 13 dpi when compared to baseline. In response to l -NAME treatment, atrium tissue levels of ACE1 were significantly reduced in treated animals at day 17, while Angiotensin-(1–7) concentration in atrium significantly increased in this group at the same time-point. No changes were detected in RAS components in the ventricle. ACE2 levels in Soleus muscle were significantly reduced in treated animals at day 13. In conclusion, changes in RAS molecules were detected during acute phase of T. cruzi infection and the inhibition of NO synthesis clearly interfered with expression of ACE1 and Angiotensin-(1–7) in the atrium.