Title:Hormone-Dependent Regulation of Renin and Effects on Prorenin
Receptor Signaling in the Collecting Duct
Volume: 18
Issue: 2
Author(s): Lucienne S. Lara, Alexis A. Gonzalez, Matthew T. Hennrikus and Minolfa C. Prieto*
Affiliation:
- Department of Physiology, Tulane University School of Medicine, New Orleans, LA, USA
- Tulane Renal and Hypertension Center of Excellence, Tulane University School of Medicine, New Orleans, LA, USA
Keywords:
Intrarenal angiotensin II, vasopressin, bradykinin, prostaglandins, protein kinase, nitric oxide.
Abstract: The production of renin by the principal cells of the collecting duct has widened our
understanding of the regulation of intrarenal angiotensin II (Ang II) generation and blood pressure.
In the collecting duct, Ang II increases the synthesis and secretion of renin by mechanisms involving
the activation of Ang II type 1 receptor (AT1R) via stimulation of the PKCα, Ca2+, and
cAMP/PKA/CREB pathways. Additionally, paracrine mediators, including vasopressin (AVP),
prostaglandins, bradykinin (BK), and atrial natriuretic peptide (ANP), regulate renin in principal
cells. During Ang II-dependent hypertension, despite plasma renin activity suppression, renin and
prorenin receptor (RPR) are upregulated in the collecting duct and promote de novo formation of
intratubular Ang II. Furthermore, activation of PRR by its natural agonists, prorenin and renin,
may contribute to the stimulation of profibrotic factors independent of Ang II. Thus, the interactions
of RAS components with paracrine hormones within the collecting duct enable tubular compartmentalization
of the RAS to orchestrate complex mechanisms that increase intrarenal Ang II,
Na+ reabsorption, and blood pressure.
