Controlled Hemorrhage Sensitizes Angiotensin II-Elicited Hypertension through Activation of the Brain Renin-Angiotensin System Independently of Endoplasmic Reticulum Stress

Guo-Biao Wu; Hui-Bo Du; Jia-Yi Zhai; Si Sun; Jun-Ling Cui; Yang Zhang; Zhen-Ao Zhao; Jian-Liang Wu; Alan Kim Johnson; Baojian Xue; Zi-Gang Zhao; Geng-Shen Zhang

doi:10.1155/2022/6371048

Back

Controlled Hemorrhage Sensitizes Angiotensin II-Elicited Hypertension through Activation of the Brain Renin-Angiotensin System Independently of Endoplasmic Reticulum Stress

Journal article

Open access

Peer reviewed

Controlled Hemorrhage Sensitizes Angiotensin II-Elicited Hypertension through Activation of the Brain Renin-Angiotensin System Independently of Endoplasmic Reticulum Stress

Guo-Biao Wu, Hui-Bo Du, Jia-Yi Zhai, Si Sun, Jun-Ling Cui, Yang Zhang, Zhen-Ao Zhao, Jian-Liang Wu, Alan Kim Johnson, Baojian Xue, …

Oxidative medicine and cellular longevity, Vol.2022, pp.6371048-6371048

01/13/2022

DOI: 10.1155/2022/6371048

PMCID: PMC8776443

PMID: 35069977

Files and links (1)

url

https://doi.org/10.1155/2022/6371048View

Published (Version of record) Open Access

Abstract

Hemorrhagic shock is associated with activation of renin-angiotensin system (RAS) and endoplasmic reticulum stress (ERS). Previous studies demonstrated that central RAS activation produced by various challenges sensitizes angiotensin (Ang) II-elicited hypertension and that ERS contributes to the development of neurogenic hypertension. The present study investigated whether controlled hemorrhage could sensitize Ang II-elicited hypertension and whether the brain RAS and ERS mediate this sensitization. Results showed that hemorrhaged (HEM) rats had a significantly enhanced hypertensive response to a slow-pressor infusion of Ang II when compared to sham HEM rats. Treatment with either angiotensin-converting enzyme (ACE) 1 inhibitor, captopril, or ACE2 activator, diminazene, abolished the HEM-induced sensitization of hypertension. Treatment with the ERS agonist, tunicamycin, in sham HEM rats also sensitized Ang II-elicited hypertension. However, blockade of ERS with 4-phenylbutyric acid in HEM rats did not alter HEM-elicited sensitization of hypertension. Either HEM or ERS activation produced a greater reduction in BP after ganglionic blockade, upregulated mRNA and protein expression of ACE1 in the hypothalamic paraventricular nucleus (PVN), and elevated plasma levels of Ang II but reduced mRNA expression of the Ang-(1-7) receptor, Mas-R, and did not alter plasma levels of Ang-(1-7). Treatment with captopril or diminazene, but not phenylbutyric acid, reversed these changes. No treatments had effects on PVN protein expression of the ERS marker glucose-regulated protein 78. The results indicate that controlled hemorrhage sensitizes Ang II-elicited hypertension by augmenting RAS prohypertensive actions and reducing RAS antihypertensive effects in the brain, which is independent of ERS mechanism.

Details

Title: Subtitle: Controlled Hemorrhage Sensitizes Angiotensin II-Elicited Hypertension through Activation of the Brain Renin-Angiotensin System Independently of Endoplasmic Reticulum Stress
Creators: Guo-Biao Wu - Departments of Neurosurgery and Medical EquipmentSecond HospitalHebei Medical UniversityShijiazhuang CityHebeiChinahebmu.edu.cn
Hui-Bo Du - Institute of MicrocirculationHebei Key Laboratory of Critical Disease Mechanism and InterventionHebei North UniversityZhangjiakou CityHebeiChinahebeinu.edu.cn
Jia-Yi Zhai - Department of Psychological and Brain SciencesUniversity of IowaIowa CityIAUSAuiowa.edu
Si Sun - Departments of Neurosurgery and Medical EquipmentSecond HospitalHebei Medical UniversityShijiazhuang CityHebeiChinahebmu.edu.cn
Jun-Ling Cui - Departments of Neurosurgery and Medical EquipmentSecond HospitalHebei Medical UniversityShijiazhuang CityHebeiChinahebmu.edu.cn
Yang Zhang - Departments of Neurosurgery and Medical EquipmentSecond HospitalHebei Medical UniversityShijiazhuang CityHebeiChinahebmu.edu.cn
Zhen-Ao Zhao - Institute of MicrocirculationHebei Key Laboratory of Critical Disease Mechanism and InterventionHebei North UniversityZhangjiakou CityHebeiChinahebeinu.edu.cn
Jian-Liang Wu - Departments of Neurosurgery and Medical EquipmentSecond HospitalHebei Medical UniversityShijiazhuang CityHebeiChinahebmu.edu.cn
Alan Kim Johnson - Department of Psychological and Brain SciencesUniversity of IowaIowa CityIAUSAuiowa.edu
Baojian Xue - Department of Psychological and Brain SciencesUniversity of IowaIowa CityIAUSAuiowa.edu
Zi-Gang Zhao - Institute of MicrocirculationHebei Key Laboratory of Critical Disease Mechanism and InterventionHebei North UniversityZhangjiakou CityHebeiChinahebeinu.edu.cn
Geng-Shen Zhang - Departments of Neurosurgery and Medical EquipmentSecond HospitalHebei Medical UniversityShijiazhuang CityHebeiChinahebmu.edu.cn
Contributors: Laura Bravo (Editor)
Resource Type: Journal article
Publication Details: Oxidative medicine and cellular longevity, Vol.2022, pp.6371048-6371048
DOI: 10.1155/2022/6371048
PMID: 35069977
PMCID: PMC8776443
NLM abbreviation: Oxid Med Cell Longev
ISSN: 1942-0900
eISSN: 1942-0994
Publisher: Hindawi
Grant note: 81670446 / National Natural Science Foundation of China 303132618 / Funds for Prevention of Geriatric Diseases of Hebei Province R01 HL-139575 / National Institutes of Health
Language: English
Date published: 01/13/2022
Academic Unit: Psychological and Brain Sciences; Neuroscience and Pharmacology; Neurology (Pediatrics); Health, Sport, and Human Physiology
Record Identifier: 9984213417002771

Metrics

8 Record Views

4 Times Cited - Web of Science