Role of the kidney in the pathogenesis of hypertension

Numerous evidence supports the notion that the kidney participates critically in the development of hypertension through various mechanisms, whether there is evidence of nephropathy (such as nephrogenic hypertension), the absence (in the case of hypertension essential). The main renal pressor mechanism is related to the inability of the kidney to excrete adequate amounts of sodium when the renal perfusion pressure is normal. Therefore, a normal perfusion pressure sodium excretion is less than the intake, creating a positive balance of sodium in the long run it increases systemic blood pressure and renal perfusion pressure to increase balance and the natriuresis sodium balance. The origin of tubular sodium hiperreabsorcion that triggers this process is invoked several types of mechanisms: 1) Excessive afferent vasoconstriction, 2) Decreased congenital or acquired from the surface of glomerular filtration, 3) excessive sodium reabsorption by subject genetic factors or by the existence of tubular alterations induced by inflammatory cells infiltrating the interstitium. Other evidence suggests that the kidney may increase blood pressure through mechanisms that directly increase peripheral resistance: the inappropriate activation SRAA, increased sympathetic tone, or impairment of endothelial function and composition of the arterial wall. All these mechanisms described above are particularly important when the treatment plant renal function is impaired and explain the increased prevalence of hypertension in our society.