Soluble (Pro)Renin Receptor in Hypertension

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Abstract

The (pro)renin receptor (PRR) was originally cloned as a specific single-transmembrane receptor for prorenin and renin and has now emerged as a multifunctional protein implicated in a wide variety of developmental and physiopathological processes. Activation of PRR in the kidney causes Na<sup>+</sup> and water retention, contributing to elevation of blood pressure in response to various hypertensive stimuli. Part of the renal action of PRR depends on activation of intrarenal renin-angiotensin system. In recent years, accumulating evidence suggests that the prohypertensive action of renal PRR was largely mediated by production of the 28-kDa soluble (pro)renin receptor through protease-mediated cleavage of the extracellular domain of PRR. The generation of multiple isoforms of PRR due to the protease-mediated cleavage partially explains diversified actions of PRR. The current review will summarize recent advances in understanding the roles of sPPR in animal models of hypertension.

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Most cited references 96

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Obesity-induced hypertension: role of sympathetic nervous system, leptin, and melanocortins.

John E Hall, Alexandre da Silva, Jussara M do Carmo … (2010)

Excess weight gain contributes to increased blood pressure in most patients with essential hypertension. Although the mechanisms of obesity hypertension are not fully understood, increased renal sodium reabsorption and impaired pressure natriuresis play key roles. Several mechanisms contribute to altered kidney function and hypertension in obesity, including activation of the sympathetic nervous system, which appears to be mediated in part by increased levels of the adipocyte-derived hormone leptin, stimulation of pro-opiomelanocortin neurons, and subsequent activation of central nervous system melanocortin 4 receptors.

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Obesity, hypertension, and chronic kidney disease

Michael Hall, Jussara M do Carmo, Alexandre A. Da Silva … (2014)

Obesity is a major risk factor for essential hypertension, diabetes, and other comorbid conditions that contribute to development of chronic kidney disease. Obesity raises blood pressure by increasing renal tubular sodium reabsorption, impairing pressure natriuresis, and causing volume expansion via activation of the sympathetic nervous system and renin–angiotensin–aldosterone system and by physical compression of the kidneys, especially when there is increased visceral adiposity. Other factors such as inflammation, oxidative stress, and lipotoxicity may also contribute to obesity-mediated hypertension and renal dysfunction. Initially, obesity causes renal vasodilation and glomerular hyperfiltration, which act as compensatory mechanisms to maintain sodium balance despite increased tubular reabsorption. However, these compensations, along with increased arterial pressure and metabolic abnormalities, may ultimately lead to glomerular injury and initiate a slowly developing vicious cycle that exacerbates hypertension and worsens renal injury. Body weight reduction, via caloric restriction and increased physical activity, is an important first step for management of obesity, hypertension, and chronic kidney disease. However, this strategy may not be effective in producing long-term weight loss or in preventing cardiorenal and metabolic consequences in many obese patients. The majority of obese patients require medical therapy for obesity-associated hypertension, metabolic disorders, and renal disease, and morbidly obese patients may require surgical interventions to produce sustained weight loss.

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Epithelial Na+ channel (ENaC), hormones, and hypertension.

James K Bubien (2010)

This minireview examines both the basic science and clinical observations over the past 20 years to show how and why overstimulation of the amiloride-sensitive epithelial Na(+) channel (ENaC) expressed by epithelial principal cells of the renal collecting duct may be responsible for a large portion of hypertension in modern society. This idea is based on the finding that, in Liddle syndrome, a mutation of the beta- and/or gamma-subunits of ENaC produces an activated ion channel, in turn resulting in severe hypertension that is resistant to most forms of conventional antihypertensive therapy. ENaC can also be stimulated to conduct sodium by two hormones: aldosterone and insulin. These hormones are both often elevated in obese individuals with therapy-resistant hypertension. Thus, overstimulation of ENaC by metabolic abnormalities in obese individuals may be a likely cause of the hypertension that accompanies obesity. The molecular mechanisms underlying both Liddle syndrome and obesity-related hypertension are different (i.e. genetic and hormonal, respectively), but both have the same end result, namely increased ENaC activity.

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Author and article information

Journal

Journal ID (publisher-id): NEF

Journal ID (nlm-ta): Nephron

Journal ID (doi): 10.1159/issn.1660-8151

Title: Nephron

Abbreviated Title: Nephron

Publisher: S. Karger AG

ISSN (Print): 1660-8151

ISSN (Electronic): 2235-3186

Publication date Subscription-year: 2023

Publication date (Print): April 2023

Publication date (Electronic): 22 July 2022

Volume: 147

Issue: 3-4

Pages: 234-243

Affiliations

Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, USA

Article

Publisher ID: 525635 Pmcid ID: PMC9867785 Other ID: Nephron 2023;147:234–243

DOI: 10.1159/000525635

PMC ID: PMC9867785

PubMed ID: 35871512

SO-VID: 8dfeb209-02c1-40ad-aabc-c06b9bf9f7a8

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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.

History

Date received : 28 January 2022

Date accepted : 27 May 2022

Page count

Figures: 2, Pages: 10

Funding

This work was supported by National Institutes of Health Grants DK104072 and DK094956, VA Merit Review from the Department of Veterans Affairs, and National Natural Science Foundation of China Grants No. 91439205 and No. 31330037. T. Yang is a Research Career Scientist in the Department of Veterans Affairs.

Soluble (Pro)Renin Receptor in Hypertension

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Karger: Nephrology

Most cited references 96

Obesity-induced hypertension: role of sympathetic nervous system, leptin, and melanocortins.

Obesity, hypertension, and chronic kidney disease

Epithelial Na+ channel (ENaC), hormones, and hypertension.

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