Nguyen Geneviève
Institut National de la Santé et de la Recherche Médicale, INSERM Unit 36, and Collège de France, Unit of Experimental Medicine, Paris, France.
Semin Nephrol. 2007 Sep;27(5):519-23. doi: 10.1016/j.semnephrol.2007.07.004.
Renin inhibitors are now available in therapeutic doses and it is accepted that they decrease blood pressure as efficiently as the classic inhibitors of the renin-angiotensin system (RAS): angiotensin converting enzyme inhibitors and angiotensin II-receptor blockers (ARBs). One major issue will be to know how, beyond the normalization of blood pressure, renin inhibitors (RIs) will compare with angiotensin converting enzyme inhibitors and ARBs for their ability to protect the organs against the tissue damage associated with overactivation of the RAS. The mechanism(s) of tissue protection may involve the inhibition of a direct cellular effect of renin and prorenin mediated by the (pro)renin receptor ([P]RR). This review updates the recent findings on (P)RR; its role in hypertension, cardiac fibrosis, diabetic nephropathy, and retinopathy; and the effects of a putative (P)RR antagonist.