AT2R and Sympathetic Outflow

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations

Abstract

Angiotensin type 2 receptor (AT2R) protein content has been demonstrated in the sympathetic regulatory regions of the brain in mature rats and mice. In the rostral ventrolateral medulla of normal animals, the AT2R tonically suppresses sympathetic tone by increasing presympathetic neuronal potassium current and therefore reducing neuronal excitability and discharge. In the chronic heart failure (CHF) state and in neurogenic hypertension, central AT2R expression is significantly downregulated. This pathological alteration of AT2R signaling contributes to sympathetic hyperactivity, a major characteristic of these two diseases. Gene transfer-induced overexpression and pharmacologically evoked activation of central AT2Rs provide a potential therapeutic strategy in the CHF and hypertension states by promoting sympathetic inhibition.

Original languageEnglish (US)
Title of host publicationThe Protective Arm of the Renin Angiotensin System (RAS)
Subtitle of host publicationFunctional Aspects and Therapeutic Implications
PublisherElsevier Inc.
Pages109-118
Number of pages10
ISBN (Electronic)9780128014851
ISBN (Print)9780128013649
DOIs
StatePublished - Apr 22 2015

Keywords

  • Angiotensin type 2 receptor
  • Chronic heart failure
  • Compound 21
  • Neurogenic hypertension
  • Neuronal -potassium channel
  • Neuronal discharge
  • Presympathetic neurons
  • Renal sympathetic nerve activity
  • Rostral ventrolateral medulla
  • Sympathetic regulation

ASJC Scopus subject areas

  • Medicine(all)

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  • Cite this

    Gao, L., & Zucker, I. H. (2015). AT2R and Sympathetic Outflow. In The Protective Arm of the Renin Angiotensin System (RAS): Functional Aspects and Therapeutic Implications (pp. 109-118). Elsevier Inc.. https://doi.org/10.1016/B978-0-12-801364-9.00015-8