RESUMO
Inflammation is recognized as an important factor in the pathophysiology of hypertension, with the renin-angiotensin-aldosterone system (RAAS) playing a key role in the disease. Initially described because of its contribution to extracellular fluid and electrolyte homeostasis, the RAAS has been implicated in endothelial dysfunction, vascular remodeling, oxidative stress, proinflammatory cytokine production, and adhesion molecule synthesis by the vascular wall. Both angiotensin II and aldosterone are involved in these systemic effects, activating innate and adaptive immune responses. This paper highlights some aspects connecting RAAS to the hypertensive phenotype, based on experimental and clinical studies, with emphasis on new findings regarding the contribution of an increasingly studied population of T lymphocytes: the T-regulatory lymphocytes. These cells can suppress inflammation and may exert beneficial vascular effects in animal models of hypertension.
RESUMO
Endothelial dysfunction is one of the main characteristics of chronic hypertension and it is characterized by impaired nitric oxide (NO) bioactivity determined by increased levels of reactive oxygen species. Endothelial function is usually evaluated by measuring the vasodilation induced by the local NO production stimulated by external mechanical or pharmacological agent. These vascular reactivity tests may be carried out in different models of experimental hypertension such as NO-deficient rats, spontaneously hypertensive rats, salt-sensitive rats, and many others. Wire myograph and pressurized myograph are the principal methods used for vascular studies. Usually, increasing concentrations of the vasodilator acetylcholine are added in cumulative manner to perform endothelium-dependent concentration-response curves. Analysis of vascular mechanics is relevant to identify arterial stiffness. Both endothelial dysfunction and vascular stiffness have been shown to be associated with increased cardiovascular risk.
RESUMO
O objetivo do tratamento anti-hipertensivo é reduzir a morbidade e a mortalidade cardiovascular. Para isso, o principal é reduzir os níveis de pressão arterial. Entretanto, a abordagem dos fatores de risco e o controle das condições clínicas associadas também são necessários para definir a meta de pressão arterial a ser atingida. De maneira geral,as duas metas de pressão arterial reconhecidas por todas as diretrizes são abaixo de 140/90 mmHg para a população de hipertensos de baixo risco e abaixo de 130/80 mmHg para pacientes diabéticos ou com doença renal. Por outro lado, outros subgrupos de hipertensos são abordados de maneira diferente entre as diferentes diretrizes. Em contraste com algumas diretrizes, recentes estudos controlados randomizados e revisão sistemática indicam que uma redução mais intensa da pressão arterial não resulta na diminuição do aparecimento de eventos cardiovasculares ou da mortalidade nos indivíduos hipertensos.
The goal of antihypertensive treatment is to reduce cardiovascular morbidity and mortality. To reach this objective,the main recommendation is to reduce levels of blood pressure. However, risk factor assessment and control of associated clinical conditions are also necessary to define the blood pressure target to be reached. In general, the two blood pressure targets recognized by all the guidelines are below 140/90 mmHg for hypertensive population at low risk and below 130/80 mmHg for patients with diabetes or kidney disease. On the other hand, other subgroups of hypertensive patients are treated differently among the different guidelines. In contrast to some guidelines, recent randomized controlled trials and systematic reviews indicate that a greater reduction in blood pressure does not result in reducing the occurrence of cardiovascular events or mortality in hypertensive patients.
