Efeito vascular e central do carvacrol na hipertensão e na inibição do apetite por sódio em ratos / Vascular and central effects of carvacrol on hypertension and inhibition of sodium appetite in rats

INTRODUÇÃO: A hipertensão arterial tem sido considerada como sendo a principal causa da redução da qualidade e expectativa de vida dos indivíduos por ser importante fator de risco para doenças que envolvem a aterosclerose e a trombose com consequente acometimento cardíaco, cerebral, renal e vascular. Estudos têm demonstrado a ação dos monoterpenos em diferentes atividades farmacológicas, entre elas sobre o sistema cardiovascular. Foi observado que o carvacrol, um monoterpeno característico da família Labiateae, apresenta ação hipotensora em ratos Wistar anestesiados tratados previamente com L-NAME e em ratos não anestesiados. OBJETIVOS: a) avaliar a ação periférica do carvacrol na pressão arterial e na frequência cardíaca em animais com hipertensão arterial vascular; b) avaliar a ação periférica do carvacrol na pressão arterial e na frequência cardíaca em ratos com hipertensão renovascular; c) avaliar a ação periférica do carvacrol sobre a pressão arterial e a frequência cardíaca em ratos espontaneamente hipertensos; d) avaliar a ação central do carvacrol sobre a pressão arterial e a frequência cardíaca em animais espontaneamente hipertensos; e) avaliar a ação central do carvacrol no apetite por sódio em animais espontaneamente hipertensos. MATERIAL E MÉTODOS: Foram utilizados ratos Wistar (200-250g)...

INTRODUCTION: Hypertension has been regarded as the primary cause of the reduction of the quality and life expectancy of individuals for being important factor ate risk for diseases that involve the atherosclerosis and thrombosis with consequent cardiac involvement, cerebral, renal and vascular. Studies have demonstrated the action of monoterpenes in different pharmacological activities, among them on the cardiovascular system. It was observed that the carvacrol, a characteristic of the monoterpene Labiateae family, presents hypotensive action in anesthetized Wistar rats pretreated with L-NAME and not anesthetized rats. AIM: a) evaluate the peripheral action of carvacrol on blood pressure and heart rate in animals with vascular arterial hypertension; b) evaluate the peripheral action of carvacrol on blood pressure and heart rate in rats with renovascular hypertension; c) evaluate the peripheral action of carvacrol on blood pressure and heart rate in animals spontaneously hypertensive; d) evaluate the central action of carvacrol on blood pressure and heart rate in animals spontaneously hypertensive; e) evaluate the action of carvacrol in central appetite for sodium in spontaneosuly hypertensive. MATERIALS AND METHODS: Were used Wistar rats (200-250g)...

Regulation of Giα Protein Expression by Vasoactive Peptides in Hypertension: Molecular Mechanisms.

Guanine nucleotide regulatory proteins (G proteins) play a key role in the regulation of various signal transduction systems, including adenylyl cyclase/cAMP and phospholipase C (PLC)/phosphatidyl inositol (PI) turnover, which are implicated in the modulation of a variety of physiological functions, such as platelet functions, including platelet aggregation, secretion, and clot formation and cardiovascular functions, including arterial tone and reactivity. Several abnormalities in adenylyl cyclase activity, cAMP levels and G proteins have been shown to be responsible for the altered cardiac performance and vascular functions observed in cardiovascular disease states. The enhanced or unaltered levels of inhibitory G proteins (Giα) and mRNA have been reported in different models of hypertension, whereas Gsα levels are shown to be unaltered. The enhanced levels of Giα proteins precede the development of blood pressure and suggest that overexpression of Gi proteins may be one of the contributing factors for the pathogenesis of hypertension. The levels of vasoactive peptides including ET-1 and Ang II and growth factors are augmented in hypertension and contribute to the enhanced expression of Giα proteins in hypertension. In addition, oxidative stress due to enhanced levels of Ang II and ET-1 is enhanced in hypertension and may also be responsible for the enhanced expression of Giα proteins observed in hypertension. Furthermore, Ang II- and ET-1-induced transactivation of growth factor receptor through the activation of MAP kinase signaling is also shown to contribute to the augmented levels of Giα in hypertension. Thus, it appears that the enhanced levels of vasoactive peptides by increasing oxidative stress and transactivation growth factor receptors enhance MAP kinase activity that contribute to the enhanced expression of Giα proteins responsible for the pathogenesis of hypertension. In this review, we describe the role of vasoactive peptides and the signaling mechanisms responsible for the enhanced expression of Giα proteins in hypertension.

¿Es la hipertensión sensible a sal una enfermedad inflamatoria?: Papel de los linfocitos y macrófagos / Is salt sensitive hypertension an inflammatory disease?: Role of lymphocytes and macrophages

La hipertensión arterial sistémica es un problema de salud pública. Esta entidad afecta al 43% de la población mexicana y es considerada una de los principales factores de riesgo para el desarrollo de eventos vasculares cerebrales, insuficiencia cardiaca e insuficiencia renal. La prevalencia de hipertensión arterial sistémica se ha incrementado durante las últimas décadas debido a la adopción de una dieta alta en sal. Existe evidencia de que la hipertensión sensible a sal se acompaña de alteraciones estructurales renales como dilatación tubular, fibrosis intersticial en parches, expresión de osteopontina e infiltrado túbulo intersticial de linfocitos y macrófagos, que impiden una excreción urinaria de sodio adecuada y en consecuencia, favorecen el desarrollo de HAS. De forma experimental se ha demostrado que estas alteraciones estructurales tienen una naturaleza inflamatoria y que la administración de medicamentos inmunosupresores disminuye la lesión tisular y mejoran el control de la presión arterial. En conjunto, los conocimientos derivados de los estudios de hipertensión sensible a sal pueden derivar en el desarrollo de nuevos fármacos destinados a mejorar el pronóstico asociado a la hipertensión arterial sistémica.

High blood pressure is a public health problem. This entity affects 43% of the mexican population and is considered a major risk factor for development of stroke, cardiac failure and chronic kidney disease. Hypertension prevalence has increased over the last decades, mainly because of high salt diet. There is evidence showing that salt-sensitive hypertension develops structural changes as tubular dilation, patchy interstitial fibrosis, osteopontin expression and lymphocytic/macrophage tubulointerstitial infiltrate that blunts urinary sodium excretion and therefore promotes HBP. It has been shown that this structural damage has an inflammatory origin and that immunosuppresant drugs down-regulates tissular injury and improves blood pressure control. In summary, this salt-sentitive hypertension data can be used in development of new and potent blood pressure drugs.

Efeitos cardiovasculares da transferência adotiva de linfócitos T reguladores em camundongos submetidos à infusão crônica de angiotensina II e de aldosterona / Cardiovascular effects of adoptive transfer of regulatory T lymphocytes in mice submitted to chronic infusion of angiotensin II and aldosterone

A angiotensina (Ang) II e aldosterona induzem hipertensão arterial por mecanismos em parte mediados pela imunidade adaptativa, envolvendo linfócitos T auxiliares respondedores (Tresp). Os linfócitos T reguladores (Treg) são capazes de suprimir os efeitos pró-inflamatórios do sistema imune. O presente estudo avaliou se a transferência adotiva de Treg é capaz de prevenir a hipertensão e a lesão vascular induzidas pela AngII ou pela aldosterona, em dois protocolos distintos. No protocolo com Ang II, camundongos machos C57BL/6 sofreram a injeção endovenosa de Treg ou Tresp, sendo depois infundidos com Ang II (1ug/kg/min), ou salina (grupo controle) por 14 dias. No protocolo com aldosterona, um outro conjunto de animais sofreu injeções de Treg ou Tresp, sendo depois infundido com aldosterona (600ug/kg/d) ou salina (grupo controle), pelo mesmo intervalo de tempo. O grupo tratado com aldosterona recebeu salina 1% na água. Tanto o grupo Ang II como aldosterona apresentaram elevação da pressão arterial sistólica (43% e 31% respectivamente), da atividade da NADPH oxidase na aorta (1,5 e 1,9 vezes, respectivamente) e no coração (1,8 e 2,4 vezes, respectivamente) e uma redução da resposta vasodilatadora à acetilcolina (de 70% e 56%, respectivamente), quando comparados com os respectivos controles (P<0,05). Adicionalmente, a administração de Ang II proporcionou um aumento rigidez vascular (P<0,001), na expressão de VCAM-1 nas artérias mesentéricas (P<0,05), na infiltração aórtica de macrófagos e linfócitos T (P<0,001) e nos níveis plasmáticos das citocinas inflamatórias interferon (INF)-y, interleucina (IL)-6, Tumor necrosis factor (TNF)-a e IL-10 (P<0,05). Ang II causou uma queda de 43% no número de células Foxp3+ no córtex renal, enquanto que a transferência adotiva de Treg aumentou as células Foxp3+ em duas vezes em comparação com o controle. A administração de Treg preveniu o remodelamento vascular induzido pela aldosterona, observado na relação média/lúmen...

Angiotensin (Ang) II and aldosterone (aldo) induce hypertension through mechanisms in part mediated by adaptive immunity and T responder lymphocytes. T regulatory (Treg) lymphocytes suppress pro-inflammatory mediators of the immune system. We questioned whether Treg adoptive transfer will blunt Ang II or aldo-induced hypertension and vascular injury, by evaluating two distinct protocols. In the Ang II protocol, male C57BL/6 mice were injected i.v. with Treg or T responder cells, and then infused with Ang II (1ug/kg/min) or saline, for 14 days. In the aldosterone protocol, another set of animals was injected with Treg or T responder cells, and then infused with aldosterone (600ug/kg/d) or saline, for the same period. The aldosterone group received saline 1% in drinking water. Both Ang II and aldosterone treated mice presented an increase in systolic blood pressure (43% and 31% respectively), of NADPH oxidase activity in aorta (1.5 and 1.9 fold, respectively) and heart (1.8 and 2.4 fold respectively) and an impaired vasodilatory response do acetylcholine (by 70% and 56% respectively), when compared to their controls (P<0.05). In addition, Ang II administration resulted in increased vascular stiffness (P<0.001), mesenteric artery vascular cell adhesion molecule (VCAM-1) expression (P<0.05), aortic macrophage and T cell infiltration (P<0.001), and the plasma levels of the inflammatory cytokines INF-y, IL-6, TNF-a, and IL-10 (P<0,05). And II caused a 43% decrease in the number of Foxp3+ cells in the renal cortex, while Treg adoptive transfer increased Foxp3+ cells 2-fold compared to control. Treg administration prevented aldosterone-induced vascular remodelling, as observed by media to lumen ratio and media cross sectional area analysis of mesenteric arteries (P<0,05). All the above were prevented by Treg but not by T responder cell adoptive transfer. These results demonstrate that Treg suppress Ang II of aldo-mediated vascular injury and BP elevation...

A aplicabilidade da medicina do sono nas emergências médicas e cardiológicas / The study of sleep disorders medicine in patients with cardiologic problems has observed special attention in the last year

Este artigo enfoca a contribuição que a medicina do sono tem proporcionado à abordagem do paciente na sala de emergência, onde, nos últimos anos, cresceu o interesse por este tema. Descreve a fisiologia cardiovascular durante o sono, delineia a relação dos distúrbios do sono com determinadas entidades cardiológicas e com os acidentes de trânsito. Esta revisão focaliza a necessidade do conhecimento das desordens do sono, para que o médico emergencista proporcione melhor qualidade no atendimento

El feto y su entorno: factores que se asocian a hipertensión arterial esencial / The fetus and his environment: associated factors to essential arterial hypertension

Se efectúa una revisión concerniente a la relación entre hipertensión arterial esencial (HEs) y su origen en la vida fetal. Entre los diferentes trabajos destaca el de Kotchen y cols. quienes realizan un estudio en madres adolescentes con HE durante el embarazo y cuyos resultados revelan una PA de los hijos entre el tercer y sexto año de vida superior al del grupo control. Dichos resultados son confirmados por otros autores (Palti y Seidman). Resulta interesante el estudio de law y su grupo quienes sugieren una posible interacción entre fenómenos fetales y maternales como determinantes de la PA del adulto. En suma esta revisión nos conduce a considerar la importancia de la interacción madre y feto como posibles factores patogénicos de la HEs

Effect of pregnancy associated hypertension on immunoglobulin levels in newborns.

In a prospective study of 124 neonates born to mothers with normal pregnancy and pregnancy associated hypertension (PAH), serum IgG, IgA and IgM were estimated by single radial immunodiffusion technique. Significantly low levels of IgG were found in mothers having PAH, as compared to normal pregnancy (p less than 0.001), whereas IgA and IgM showed no difference in the two groups. There was no statistical difference in maternal and cord blood IgG in either the control or study group. IgG was significantly higher (p less than 0.001) in cord blood of babies born by vaginal route as compared to forceps (via vaginal route) or cesarean section. IgA and IgM levels did not vary with mode of delivery.