Níveis séricos de mediadores inflamatórios da resposta imune na gênese da hipertensão essencial

Abstract

Systemic hypertension (SH) is characterized by a persistently elevated blood pressure levels to values above 140 by 90 mmHg. It presents as a chronic degenerative disease, multifactorial, compromising the vasodilator and vasoconstrictor systems. Its primary hemodynamic marker is the persistent increase in peripheral vascular resistance. Is frequently associated with functional and/or structural changes in target organs. In the last 20 years, population surveys in Brazilian cities showed the prevalence of hypertension above 30%. Outperforms other cardiovascular risk factors such as smoking, hypercholesterolemia and obesity. The high BP is the main factor of risk worldwide, accounting for 9 million deaths. Some studies support the concept that this disease has immunological basis. The immune system (SI) is an effective system of defense against microorganisms or against the malignant transformation of cells. In early 2000, a series of investigations showing that the nuclear transcription factor kappa B (NF-ᴋB) and reactive oxygen species are paramount in determining lesion of target organs induced by angiotensin II. The ANG II exerts various actions that contribute to vascular damage, modulating the release of cytokines and pro-inflammatory transcription factors such as NF-ᴋB. The inflammatory and apoptotic processes can induce changes in cardiac function, in the peripheral vascular resistance, in the mechanisms of the kidneys and in plasma volume. The inflammatory molecules and certain cytokines are predictive for future cardiovascular events. In this study we quantified, by enzyme immune assay, the serum levels of inflammatory mediators and TNR receptor family (IL-1β, IL-4, IL-12, IL-15, TNFRI, TNFRII and TRAIL) in 24 patients with SAH and 25 controls. Risk factors such as diabetes, smoking, obesity and hypercholesterolemia were criteria of exclusion. Cytokines and soluble TNF-α receptors showed no significant differences between the hypertensive group and controls. These data suggest that the analyzed mediators do not participate in the genesis in the onset essential hypertension.