Estrogen regulation of the brain renin-angiotensin system in protection against angiotensin II-induced sensitization of hypertension

Baojian Xue; Zhongming Zhang; Terry G Beltz; Fang Guo; Meredith Hay; Alan Kim Johnson

doi:10.1152/ajpheart.01012.2013

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Estrogen regulation of the brain renin-angiotensin system in protection against angiotensin II-induced sensitization of hypertension

Journal article

Open access

Estrogen regulation of the brain renin-angiotensin system in protection against angiotensin II-induced sensitization of hypertension

Baojian Xue, Zhongming Zhang, Terry G Beltz, Fang Guo, Meredith Hay and Alan Kim Johnson

American journal of physiology. Heart and circulatory physiology, Vol.307(2), pp.H191-H198

07/15/2014

DOI: 10.1152/ajpheart.01012.2013

PMCID: PMC4101642

PMID: 24858844

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Abstract

This study investigated sex differences in the sensitization of angiotensin (ANG) II-induced hypertension and the role of central estrogen and ANG-(1-7) in this process. Male and female rats were implanted for telemetered blood pressure (BP) recording. A subcutaneous subpressor dose of ANG II was given alone or concurrently with intracerebroventricular estrogen, ANG-(1-7), an ANG-(1-7) receptor antagonist A-779 or vehicle for 1 wk (induction). After a 1-wk rest (delay), a pressor dose of ANG II was given for 2 wk (expression). In males and ovariectomized females, subpressor ANG II had no sustained effect on BP during induction, but produced an enhanced hypertensive response to the subsequent pressor dose of ANG II during expression. Central administration of estrogen or ANG-(1-7) during induction blocked ANG II-induced sensitization. In intact females, subpressor ANG II treatment produced a decrease in BP during induction and delay, and subsequent pressor ANG II treatment given during expression produced only a slight but significant increase in BP. However, central blockade of ANG-(1-7) by intracerebroventricular infusion of A-779 during induction restored the decreased BP observed in females during induction and enhanced the pressor response to the ANG II treatment during expression. RT-PCR analyses indicated that estrogen given during induction upregulated mRNA expression of the renin-angiotensin system (RAS) antihypertensive components, whereas both central estrogen and ANG-(1-7) downregulated mRNA expression of RAS hypertensive components in the lamina terminalis. The results indicate that females are protected from ANG II-induced sensitization through central estrogen and its regulation of brain RAS.

Estrogen Replacement Therapy

Angiotensin II - administration & dosage

Receptors, G-Protein-Coupled - metabolism

Male

RNA, Messenger - metabolism

Brain - metabolism

Peptidyl-Dipeptidase A - genetics

Receptor, Angiotensin, Type 1 - genetics

Time Factors

Peptidyl-Dipeptidase A - metabolism

Hypertension - prevention & control

Female

Blood Pressure - drug effects

Hypertension - genetics

Receptor, Angiotensin, Type 1 - drug effects

Receptors, G-Protein-Coupled - drug effects

Disease Models, Animal

Proto-Oncogene Proteins - metabolism

Proto-Oncogene Proteins - drug effects

Ovariectomy

Brain - physiopathology

Peptide Fragments - administration & dosage

Angiotensin I - administration & dosage

Estradiol - administration & dosage

Gene Expression Regulation

Rats

Proto-Oncogene Proteins - genetics

Renin-Angiotensin System - genetics

Angiotensin II - analogs & derivatives

Telemetry

Rats, Sprague-Dawley

Hypertension - physiopathology

Hypertension - metabolism

Brain - drug effects

Animals

Receptor, Angiotensin, Type 1 - metabolism

Sex Factors

Renin-Angiotensin System - drug effects

Receptors, G-Protein-Coupled - genetics

Infusions, Intraventricular

Details

Title: Subtitle: Estrogen regulation of the brain renin-angiotensin system in protection against angiotensin II-induced sensitization of hypertension
Creators: Baojian Xue - Department of Psychology, University of Iowa, Iowa City, Iowa; baojian-xue@uiowa.edu
Zhongming Zhang - Zhang Zhongjing College of Chinese Medicine, Nanyang Institute of Technology, Henan, China
Terry G Beltz - Department of Psychology, University of Iowa, Iowa City, Iowa
Fang Guo - Department of Psychology, University of Iowa, Iowa City, Iowa
Meredith Hay - Department of Physiology, University of Arizona, Tucson, Arizona; Evelyn F. McKnight Brain Institute, University of Arizona, Tucson, Arizona; and
Alan Kim Johnson - Department of Psychology, University of Iowa, Iowa City, Iowa; Department of Pharmacology, University of Iowa, Iowa City, Iowa; Francois M. Abboud Cardiovascular Research Center, University of Iowa, Iowa City, Iowa
Resource Type: Journal article
Publication Details: American journal of physiology. Heart and circulatory physiology, Vol.307(2), pp.H191-H198
DOI: 10.1152/ajpheart.01012.2013
PMID: 24858844
PMCID: PMC4101642
NLM abbreviation: Am J Physiol Heart Circ Physiol
ISSN: 0363-6135
eISSN: 1522-1539
Publisher: United States
Grant note: P01 HL014388 / NHLBI NIH HHS MH-80241 / NIMH NIH HHS HL-14388 / NHLBI NIH HHS HL-98207 / NHLBI NIH HHS
Language: English
Date published: 07/15/2014
Academic Unit: Psychological and Brain Sciences; Neuroscience and Pharmacology; Neurology (Pediatrics); Health, Sport, and Human Physiology
Record Identifier: 9984002494902771

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