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Dimerization of AT2 and Mas Receptors in Control of Blood Pressure

  • Hypertension and the Kidney (RM Carey, Section Editor)
  • Published:
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A Correction to this article was published on 12 May 2018

This article has been updated

Abstract

Purpose of Review

Angiotensin type 2 receptor (AT2R) and receptor Mas (MasR) are part of the “protective arm” of the renin angiotensin system. Gene and pharmacological manipulation studies reveal that AT2R and MasR are involved in natriuretic, vasodilatory, and anti-inflammatory responses and in lowering blood pressure in various animal models under normal and pathological conditions such as salt-sensitive hypertension, obesity, and diabetes. The scope of this review is to discuss co-localization and heterodimerization as potential molecular mechanisms of AT2R- and MasR-mediated functions including antihypertensive activities.

Recent Findings

Accumulating evidences show that AT2R and MasR are co-localized, make a heterodimer, and are functionally interdependent in producing their physiological responses. Moreover, ang-(1-7) preferably may be an AT1R-biased agonist while acting as a MasR agonist.

Summary

The physical interactions of AT2R and MasR appear to be an important mechanism by which these receptors are involved in blood pressure regulation and antihypertensive activity. Whether heteromers of these receptors influence affinity or efficacy of endogenous or synthetic agonists remains a question to be considered.

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Change history

  • 12 May 2018

    In the original publication, the Fig. 1 caption contains an error. The original article has been corrected.

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Funding

This study was supported by NIH R01 grant DK61578.

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Correspondence to Tahir Hussain.

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The original version of this article was revised: The Fig. 1 caption contains an error

This article is part of the Topical Collection on Hypertension and the Kidney

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Patel, S., Hussain, T. Dimerization of AT2 and Mas Receptors in Control of Blood Pressure. Curr Hypertens Rep 20, 41 (2018). https://doi.org/10.1007/s11906-018-0845-3

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