COX-2-Independent Activation of Renal (Pro)Renin Receptor Contributes to DOCA-Salt Hypertension in Rats.

COX-2-Independent Activation of Renal (Pro)Renin Receptor Contributes to DOCA-Salt Hypertension in Rats. Am J Physiol Renal Physiol. 2020 Aug 17;: Authors: Wang F, Sun Y, Luo R, Lu X, Yang B, Yang T Abstract It's been shown that COX-2-dependent activation of renal (pro)renin receptor (PRR) contributes to angiotensin II (AngII)-induced hypertension. However, less is known about the involvement of this mechanism in AngII-independent hypertension. The goal of the present study was to test whether or not COX-2-dependent upregulation of PRR serves as a universal mechanism contributing to AngII-dependent and -independent hypertension. Here we examined the association between renal COX-2 and PRR during deoxycorticosterone acetate (DOCA)-salt hypertension in rats. By immunoblotting and immunofluorescence, renal protein expression of PRR was remarkably upregulated by (DOCA)-salt treatment. Surprisingly, this upregulation of renal PRR expression was unaffected by a COX-2 inhibitor celecoxib. To address the role of renal PRR to pathogenesis of DOCA-salt hypertension, a decoy PRR inhibitor PRO20 was infused to the renal medulla of uninephrectomized Sprague-Dawley rats for 14 days. Radiotelemetry demonstrated effective attenuation of DOCA-salt hypertension by intramedullary infusion of a PRR inhibitor PRO20. In parallel, DOCA-salt-induced hypertrophy in the heart and the kidney, and proteinuria were improved as well, accompanied with blunted poly...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research