Functional expression of kinin B1 and B2 receptors in mouse abdominal aorta

Previous studies have shown that the vascular reactivity of the mouse aorta differs substantially from that of the rat aorta in response to several agonists such as angiotensin II, endothelin-1 and isoproterenol. However, no information is available about the agonists bradykinin (BK) and DesArg9BK (DBK). Our aim was to determine the potential expression of kinin B1 and B2 receptors in the abdominal mouse aorta isolated from C57BL/6 mice. Contraction and relaxation responses to BK and DBK were investigated using isometric recordings. The kinins were unable to induce relaxation but concentration-contraction response curves were obtained by applying increasing concentrations of the agonists BK and DBK. These effects were blocked by the antagonists Icatibant and R-715, respectively. The potency (pD2) calculated from the curves was 7.0 ± 0.1 for BK and 7.3 ± 0.2 for DBK. The efficacy was 51 ± 2% for BK and 30 ± 1% for DBK when compared to 1 µM norepinephrine. The concentration-dependent responses of BK and DBK were markedly inhibited by the arachidonic acid inhibitor indomethacin (1 µM), suggesting a mediation by the cyclooxygenase pathway. These contractile responses were not potentiated in the presence of the NOS inhibitor L-NAME (1 mM) or endothelium-denuded aorta, indicating that the NO pathway is not involved. We conclude that the mouse aorta constitutively contains B1 and B2 subtypes of kinin receptors and that stimulation with BK and DBK induces contractile effect mediated by endothelium-independent vasoconstrictor prostanoids.

Analysis of renin-angiotensin-aldosterone system gene polymorphisms in resistant hypertension

Essential hypertension is a disease multifactorially triggered by genetic and environmental factors. The contribution of genetic polymorphisms of the renin-angiotensin-aldosterone system and clinical risk factors to the development of resistant hypertension was evaluated in 90 hypertensive patients and in 115 normotensive controls living in Southwestern Brazil. Genotyping for insertion/deletion of angiotensin-converting enzyme, angiotensinogen M235T, angiotensin II type 1 receptor A1166C, aldosterone synthase C344T, and mineralocorticoid receptor A4582C polymorphisms was performed by PCR, with further restriction analysis when required. The influence of genetic polymorphisms on blood pressure variation was assessed by analysis of the odds ratio, while clinical risk factors were evaluated by logistic regression. Our analysis indicated that individuals who carry alleles 235-T, 1166-A, 344-T, or 4582-C had a significant risk of developing resistant hypertension (P < 0.05). Surprisingly, when we tested individuals who carried the presumed risk genotypes A1166C, C344T, and A4582C we found that these genotypes were not associated with resistant hypertension. However, a gradual increase in the risk to develop resistant hypertension was detected when the 235-MT and TT genotypes were combined with one, two or three of the supposedly more vulnerable genotypes - A1166C (AC/AA), C344T (TC/TT) and A4582C (AC/CC). Analysis of clinical parameters indicated that age, body mass index and gender contribute to blood pressure increase (P < 0.05). These results suggest that unfavorable genetic renin-angiotensin-aldosterone system patterns and clinical risk variables may contribute to increasing the risk for the development of resistant hypertension in a sample of the Brazilian population.

Eccentric and concentric cardiac hypertrophy induced by exercise training: microRNAs and molecular determinants

Among the molecular, biochemical and cellular processes that orchestrate the development of the different phenotypes of cardiac hypertrophy in response to physiological stimuli or pathological insults, the specific contribution of exercise training has recently become appreciated. Physiological cardiac hypertrophy involves complex cardiac remodeling that occurs as an adaptive response to static or dynamic chronic exercise, but the stimuli and molecular mechanisms underlying transduction of the hemodynamic overload into myocardial growth are poorly understood. This review summarizes the physiological stimuli that induce concentric and eccentric physiological hypertrophy, and discusses the molecular mechanisms, sarcomeric organization, and signaling pathway involved, also showing that the cardiac markers of pathological hypertrophy (atrial natriuretic factor, β-myosin heavy chain and α-skeletal actin) are not increased. There is no fibrosis and no cardiac dysfunction in eccentric or concentric hypertrophy induced by exercise training. Therefore, the renin-angiotensin system has been implicated as one of the regulatory mechanisms for the control of cardiac function and structure. Here, we show that the angiotensin II type 1 (AT1) receptor is locally activated in pathological and physiological cardiac hypertrophy, although with exercise training it can be stimulated independently of the involvement of angiotensin II. Recently, microRNAs (miRs) have been investigated as a possible therapeutic approach since they regulate the translation of the target mRNAs involved in cardiac hypertrophy; however, miRs in relation to physiological hypertrophy have not been extensively investigated. We summarize here profiling studies that have examined miRs in pathological and physiological cardiac hypertrophy. An understanding of physiological cardiac remodeling may provide a strategy to improve ventricular function in cardiac dysfunction.

Prevention of etomidate-induced myoclonus during anesthetic induction by pretreatment with dexmedetomidine

Myoclonus induced by etomidate during induction of general anesthesia is undesirable. This study evaluated the effect of dexmedetomidine (DEX) pretreatment on the incidence and severity of etomidate-induced myoclonus. Ninety patients undergoing elective surgical procedures were randomly allocated to three groups (n=30 each) for intravenous administration of 10 mL isotonic saline (group I), 0.5 &#181;g/kg DEX in 10 mL isotonic saline (group II), or 1.0 &#181;g/kg DEX in 10 mL isotonic saline (group III) over 10 min. All groups subsequently received 0.3 mg/kg etomidate by intravenous push injection. The incidence and severity of myoclonus were recorded for 1 min after etomidate administration and the incidence of cardiovascular adverse events that occurred between the administration of the DEX infusion and 1 min after tracheal intubation was recorded. The incidence of myoclonus was significantly reduced in groups II and III (30.0 and 36.7%), compared with group I (63.3%). The incidence of severe sinus bradycardia was significantly increased in group III compared with group I (P<0.05), but there was no significant difference in heart rate in groups I and II. There were no significant differences in the incidence of low blood pressure among the 3 groups. Pretreatment with 0.5 and 1.0 &#181;g/kg DEX significantly reduced the incidence of etomidate-induced myoclonus during anesthetic induction; however, 0.5 &#181;g/kg DEX is recommended because it had fewer side effects.

Inibição do escurecimento enzimático de banana maçã minimamente processada

Objetivou-se, neste trabalho, avaliar o efeito do ácido ascórbico (AA), do cloreto de cálcio (CC), do cloridrato de L-cisteína (Cis) e EDTA, na prevenção do escurecimento enzimático de banana maçã minimamente processada. Foram utilizadas as combinações: (i) AA 1%+CC 1%+Cis 0,5%, (ii) AA 1%+CC 1%+Cis 1%, (iii) AA 1%+CC 1%+Cis 1,5% e (iv) EDTA 1%, constituindo quatro tratamentos de um delineamento inteiramente casualizado. Produtos minimamente processados não tratados quimicamente não foram analisados, considerando-se seu acentuado escurecimento e sua vida de prateleira inferior a 6 h. As bananas foram tratadas com hipoclorito de sódio, fatiadas, imersas nos tratamentos químicos, acondicionadas em embalagens rígidas envoltas com filme PVC 30 µm e armazenadas durante cinco dias a 5+1°C e 85+3% UR. Amostras foram analisadas diariamente, durante os cinco dias de armazenamento. Os tratamentos contendo AA 1%+CC 1%+Cis 1% e AA 1%+CC 1%+Cis 1,5% determinaram os maiores valores de acidez titulável e menores de pH. Observaram-se aumentos no valor a* e redução nos valores b* e L* na banana maçã minimamente processada, independente do tratamento químico, durante o armazenamento. O tratamento AA 1%+CC 1%+Cis 1,5% foi o mais efetivo na prevenção das modificações dos valores a*, b* e L*, associados à coloração das rodelas. Observou-se aumento na atividade da polifenoloxidase (PPO) e peroxidase (POD) durante o armazenamento das rodelas de banana, independente do tratamento, à exceção da redução observada na atividade da PPO, nos produtos tratados com EDTA. Os tratamentos contendo EDTA e AA 1%+CC 1%+Cis 1,5% foram os mais efetivos na contenção do aumento das atividades da PPO e POD, respectivamente.

beta-caroteno, ácido ascórbico e antocianinas totais em polpa de frutos de aceroleira conservada por congelamento durante 12 meses

Objetivou-se avaliar as alterações de b-caroteno, ácido ascórbico e antocianinas totais na polpa de frutos de clones de aceroleira conservada por congelamento. Os frutos dos clones BRS 152 (Sertaneja) BRS 235 (Apodi), BRS 236 (Cereja), BRS 237 (Roxinha), BRS 238 (Frutacor) e II 47/1 foram colhidos no estádio de maturação comercial (vermelho maduro) em Limoeiro do Norte, Ceará, Brasil, transportados para a Planta Piloto de Processamento de Frutos da Embrapa Agroindústria Tropical, despolpados, acondicionada a polpa em sacos de polietileno (100 g), congelada, mantida em freezer a -20 °C, e avaliada a cada 30 dias durante 12 meses. O experimento foi realizado em delineamento experimental inteiramente casualizado em esquema fatorial 6 x 13 (clones x tempo), com 3 repetições. A concentração de beta-caroteno foi estável no clone Cereja, enquanto, nos demais, houve decréscimo durante todo o período do experimento. Houve pequeno decréscimo no teor de ácido ascórbico em todos os clones estudados durante o armazenamento, provavelmente devido à alta acidez da polpa, que auxilia na manutenção deste nutriente. O teor de antocianinas totais foi estável nos clones Frutacor e Sertaneja, enquanto nos demais houve diminuição. O clone II 47/1 foi dentre os estudados o que apresentou maiores teores de ácido ascórbico e antocianinas totais, mantendo estas características durante todo o armazenamento. De um modo geral, os clones em que se determinou menor teor de beta-caroteno foram observadas as mais elevadas concentrações de antocianinas totais.

Resveratrol plays important role in protective mechanisms in renal disease - mini-review

Resveratrol (RESV) is a polyphenolic compound found in various plants, including grapes, berries and peanuts, and its processed foods as red wine. RESV possesses a variety of bioactivities, including antioxidant, anti-inflammatory, cardioprotective, antidiabetic, anticancer, chemopreventive, neuroprotective, renal lipotoxicity preventative, and renal protective effects. Numerous studies have demonstrated that polyphenols promote cardiovascular health. Furthermore, RESV can ameliorate several types of renal injury in animal models, including diabetic nephropathy, hyperuricemic, drug-induced injury, aldosterone-induced injury, ischemia-reperfusion injury, sepsis-related injury, and endothelial dysfunction. In addition, RESV can prevent the increase in vasoconstrictors, such as angiotensin II (AII) and endothelin-1 (ET-1), as well as intracellular calcium, in mesangial cells. Together, these findings suggest a potential role for RESV as a supplemental therapy for the prevention of renal injury.