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Renin- and Prorenin-Induced Effects in Rat Vascular Smooth Muscle Cells Overexpressing the Human (Pro)Renin Receptor: Does (Pro)Renin-(Pro)Renin Receptor Interaction Actually Occur?

Batenburg, Wendy W., Lu, Xifeng, Leijten, Frank, Maschke, Ulrike, Müller, Dominik N., Danser, A.H. Jan·2011·Hypertension
DOI 10.1161/hypertensionaha.111.180737
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Abstract

Renin/prorenin binding to the (pro)renin receptor ([P]RR) results in direct (angiotensin-independent) second-messenger activation in vitro, whereas in vivo studies in rodents overexpressing prorenin (≈400-fold) or the (P)RR do not support such activation. To solve this discrepancy, DNA synthesis, extracellular signal–regulated kinase 1/2 phosphorylation, and plasminogen-activator inhibitor 1 release were evaluated in wild-type and human (P)RR-overexpressing vascular smooth muscle cells after their incubation with 1 to 80 nmol/L of (pro)renin. Human prorenin (4 nmol/L, ie, ≈800-fold above normal) + angiotensinogen increased DNA synthesis in human (P)RR cells only in an angiotensin II type 1 receptor–dependent manner. Prorenin at this concentration also increased plasminogen-activator inhibitor 1 release via angiotensin. Prorenin alone at 4 nmol/L was without effect, but at 20 nmol/L (≈4000-fold above normal) it activated extracellular signal–regulated kinase 1/2 directly (ie, independent of angiotensin). Renin at concentrations of 1 nmol/L (≈2000-fold above normal) and higher directly stimulated DNA synthesis, extracellular signal–regulated kinase 1/2 phosphorylation, and plasminogen-activator inhibitor 1 release in wild-type and human (P)RR cells, and similar effects were seen for rat renin, indicating that they were mediated via the rat (P)RR. In conclusion, angiotensin generation depending on prorenin-(P)RR interaction may occur in transgenic rodents overexpressing prorenin several 100-fold. Direct (pro)renin-induced effects via the (P)RR require agonist concentrations that are far above the levels in wild-type and transgenic rats. Therefore, only prorenin (and not [P]RR) overexpression will result in an angiotensin-dependent phenotype, and direct renin-(P)RR interaction is unlikely to ever occur in nonrenin-synthesizing organs.

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  • The (P)RR interacts with renin/prorenin at supraphysiological concentrations that are several orders of magnitude higher than (patho)physiological concentrations, questioning the physiological relevance of the (P)RR-(pro)renin interaction.

    “The (pro)renin receptor ([P]RR) interacts with renin/prorenin (denoted as [pro]renin) at supraphysiological concentrations that are even several orders of magnitude higher than (patho)physiological concentrations, questioning the physiological relevance of the (P)RR–(pro)renin interaction.24,25”

    From (Pro)renin Receptor Inhibition Reprograms Hepatic Lipid Metabolism and Protects Mice From Diet-Induced Obesity and Hepatosteatosis (2018) · cites this paper as [24]

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Research works printed but not linked: 33

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Metadata

Authors
Batenburg, W. W., Lu, X., Leijten, F., Maschke, U., Müller, D. N., & Danser, A. H. J.
Affiliations
From the Division of Pharmacology and Vascular Medicine (W.W.B., X.L., F.L., A.H.J.D.), Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands; Max Delbrück Center for Molecular Medicine (U.M., D.N.M.), Berlin, Germany; Department of Experimental Medicine (D.N.M.), University of Erlangen-Nürnberg, Erlangen, Germany.
Venue
Hypertension
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2011-12
Volume
58
Issue
6
Pages
1111-1119
ISSN
  • 0194-911X
  • 1524-4563
DOI
10.1161/hypertensionaha.111.180737
Cited by
59
References
0
Language
en

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