Fig. 2.

The use of AT1-r receptor blockers (ARB), can induce increased AT2-r receptor stimulation with antifibrotic, antifibrotic and vasodilatory properties, and the vasoconstrictive, profibrotic, hyperproliferative and proinflammatory effects mediated by AT1-r stimulation are also blocked. Finally, after ARB administration the response to hypertrophic and inflammatory growth induced by TNF-a is significantly attenuated. Neprilisin inhibitors decrease the degradation of natriuretic peptides. Natriuretic peptides cause vasodilation by stimulating the guanylate cyclase receptor to produce cGMP natriuretic peptides that also exert anti-inflammatory and antifibrotic effects.