TY - JOUR
T1 - Hormone-Dependent Regulation of Renin and Effects on Prorenin Receptor Signaling in the Collecting Duct
AU - Lara, Lucienne S.
AU - Gonzalez, Alexis A.
AU - Henrrikus, Matthew A.
AU - Prieto, Minolfa C.
N1 - Funding Information:
The authors received funds from: 1) the National Institutes of Health (NIH-NIDDK; DK104375 grant), the Tulane SoM Faculty Pilot Program to M.C.P; 2) the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) for providing Productive Fellowship Level 2; the Carlos Chagas Filho Rio de Janeiro State Research Foundation (FAPERJ) grants E-26/171.137/2006 and E-26/111.665/ 2008 to L.S.L.; 3) the Science Without Borders grant from CNPq-Brazil, Especial Visiting Professor 420584/2013-7 to L.S.L. and M.C.P; 4) the Fondo Nacional De Ciencia y Tecnología (FONDEC-YT) 1191006 to A.A.G.; and 5) the Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP; 2017/17027-0 grant to L.S.L., A.A.G. and M.C.P.).
Publisher Copyright:
© 2022 Bentham Science Publishers.
PY - 2022/8
Y1 - 2022/8
N2 - 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 com-partmentalization of the RAS to orchestrate complex mechanisms that increase intrarenal Ang II, Na+ reabsorption, and blood pressure.
AB - 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 com-partmentalization of the RAS to orchestrate complex mechanisms that increase intrarenal Ang II, Na+ reabsorption, and blood pressure.
KW - bradykinin
KW - Intrarenal angiotensin II
KW - nitric oxide
KW - prostaglandins
KW - protein kinase
KW - vasopressin
UR - http://www.scopus.com/inward/record.url?scp=85142359294&partnerID=8YFLogxK
U2 - 10.2174/1573402118666220216105357
DO - 10.2174/1573402118666220216105357
M3 - Review article
C2 - 35170417
AN - SCOPUS:85142359294
VL - 18
SP - 91
EP - 100
JO - Current Hypertension Reviews
JF - Current Hypertension Reviews
SN - 1573-4021
IS - 2
ER -