ACE2 gene combined with exercise training attenuates central AngII/AT1 axis function and oxidative stress in a prehypertensive rat model
Angiotensin-converting enzyme 2 (ACE2) or exercise training (ExT) is beneficial to hypertension, but their combined effects remain unknown. In this study, lentivirus containing enhanced green fluorescent protein (eGFP) and were microinjected into the paraventricular nucleus (PVN) of young male spont...
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description | Angiotensin-converting enzyme 2 (ACE2) or exercise training (ExT) is beneficial to hypertension, but their combined effects remain unknown. In this study, lentivirus containing enhanced green fluorescent protein (eGFP) and
were microinjected into the paraventricular nucleus (PVN) of young male spontaneous hypertensive rats (SHRs), and SHRs were assigned into five groups: sedentary (SHR), SHR-ExT, SHR-eGFP,
gene (SHR-ACE2), and
gene combined with ExT (SHR-ACE2-ExT). Wistar-Kyoto (WKY) rats were used as a control.
gene or ExT significantly delayed the elevation of blood pressure, and the combined effect prevented the development and progression of prehypertension. Either
overexpression or ExT improved arterial baroreflex sensitivity (BRS), whereas the combined effect normalized BRS in SHR. Compared with SHR, SHR-ACE2 and SHR-ExT displayed a significantly higher level of ACE2 protein but had lower plasma norepinephrine (NE) and angiotensin II (AngII) as well as angiotensin II type 1 receptor (AT1) protein expression in the PVN. SHR-ACE2-ExT showed the largest decrease in AngII and AT1 protein expression. Reactive oxygen species (ROS) level and NADPH oxidase (NOX2 and NOX4) protein expression in PVN were also decreased in SHR-ACE2-ExT group than in SHR-ACE2 and SHR-ExT groups. It was concluded that the combined effect has effectively prevented prehypertension progression and baroreflex dysfunction in SHR, which is associated with the reduction in AngII/AT1 axis function and oxidative stress in the PVN.
Angiotensin-converting enzyme 2 (
) gene in combination with exercise training (ExT) delayed the progression of hypertension via normalizing the blunted baroreflex sensitivity (BRS) and inhibiting sympathetic nerve activity (SNA). Its underlying mechanism may be related to the inhibition of AngII/AT1 axis function and central oxidative stress in the paraventricular nucleus (PVN) of prehypertensive rats. |
doi_str_mv | 10.1152/japplphysiol.00459.2021 |
format | Article |
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were microinjected into the paraventricular nucleus (PVN) of young male spontaneous hypertensive rats (SHRs), and SHRs were assigned into five groups: sedentary (SHR), SHR-ExT, SHR-eGFP,
gene (SHR-ACE2), and
gene combined with ExT (SHR-ACE2-ExT). Wistar-Kyoto (WKY) rats were used as a control.
gene or ExT significantly delayed the elevation of blood pressure, and the combined effect prevented the development and progression of prehypertension. Either
overexpression or ExT improved arterial baroreflex sensitivity (BRS), whereas the combined effect normalized BRS in SHR. Compared with SHR, SHR-ACE2 and SHR-ExT displayed a significantly higher level of ACE2 protein but had lower plasma norepinephrine (NE) and angiotensin II (AngII) as well as angiotensin II type 1 receptor (AT1) protein expression in the PVN. SHR-ACE2-ExT showed the largest decrease in AngII and AT1 protein expression. Reactive oxygen species (ROS) level and NADPH oxidase (NOX2 and NOX4) protein expression in PVN were also decreased in SHR-ACE2-ExT group than in SHR-ACE2 and SHR-ExT groups. It was concluded that the combined effect has effectively prevented prehypertension progression and baroreflex dysfunction in SHR, which is associated with the reduction in AngII/AT1 axis function and oxidative stress in the PVN.
Angiotensin-converting enzyme 2 (
) gene in combination with exercise training (ExT) delayed the progression of hypertension via normalizing the blunted baroreflex sensitivity (BRS) and inhibiting sympathetic nerve activity (SNA). Its underlying mechanism may be related to the inhibition of AngII/AT1 axis function and central oxidative stress in the paraventricular nucleus (PVN) of prehypertensive rats.</description><identifier>ISSN: 8750-7587</identifier><identifier>ISSN: 1522-1601</identifier><identifier>EISSN: 1522-1601</identifier><identifier>DOI: 10.1152/japplphysiol.00459.2021</identifier><identifier>PMID: 35546127</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>ACE2 ; ACE2 gene ; Angiotensin ; Angiotensin I - metabolism ; Angiotensin II ; Angiotensin II - metabolism ; Angiotensin-converting enzyme 2 ; Angiotensin-Converting Enzyme 2 - metabolism ; Animal models ; Animals ; Baroreceptors ; Blood Pressure ; CYBB protein ; Fitness training programs ; Fluorescence ; Green fluorescent protein ; Hypertension ; Hypertension - metabolism ; Hypertension - therapy ; Male ; NAD(P)H oxidase ; Norepinephrine ; NOX4 protein ; Oxidative stress ; Oxidative Stress - physiology ; Paraventricular Hypothalamic Nucleus ; Paraventricular nucleus ; Peptidyl-dipeptidase A ; Physical Conditioning, Animal - physiology ; Physical training ; Prehypertension - metabolism ; Pressure effects ; Protein expression ; Proteins ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Reactive oxygen species ; Reflexes ; Training</subject><ispartof>Journal of applied physiology (1985), 2022-06, Vol.132 (6), p.1460-1467</ispartof><rights>Copyright American Physiological Society Jun 2022</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c341t-f14e8679ba58077ff895895a5e0e5fb7040cec332b251702473b926e446ab9623</citedby><cites>FETCH-LOGICAL-c341t-f14e8679ba58077ff895895a5e0e5fb7040cec332b251702473b926e446ab9623</cites><orcidid>0000-0002-1025-2290 ; 0000-0002-0570-4117</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3025,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35546127$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Xiu-Yun</creatorcontrib><creatorcontrib>Lin, Cheng</creatorcontrib><creatorcontrib>Liu, Guo-Ying</creatorcontrib><creatorcontrib>Pei, Chun</creatorcontrib><creatorcontrib>Xu, Gui-Qing</creatorcontrib><creatorcontrib>Gao, Lie</creatorcontrib><creatorcontrib>Wang, Shi-Zhong</creatorcontrib><creatorcontrib>Pan, Yan-Xia</creatorcontrib><title>ACE2 gene combined with exercise training attenuates central AngII/AT1 axis function and oxidative stress in a prehypertensive rat model</title><title>Journal of applied physiology (1985)</title><addtitle>J Appl Physiol (1985)</addtitle><description>Angiotensin-converting enzyme 2 (ACE2) or exercise training (ExT) is beneficial to hypertension, but their combined effects remain unknown. In this study, lentivirus containing enhanced green fluorescent protein (eGFP) and
were microinjected into the paraventricular nucleus (PVN) of young male spontaneous hypertensive rats (SHRs), and SHRs were assigned into five groups: sedentary (SHR), SHR-ExT, SHR-eGFP,
gene (SHR-ACE2), and
gene combined with ExT (SHR-ACE2-ExT). Wistar-Kyoto (WKY) rats were used as a control.
gene or ExT significantly delayed the elevation of blood pressure, and the combined effect prevented the development and progression of prehypertension. Either
overexpression or ExT improved arterial baroreflex sensitivity (BRS), whereas the combined effect normalized BRS in SHR. Compared with SHR, SHR-ACE2 and SHR-ExT displayed a significantly higher level of ACE2 protein but had lower plasma norepinephrine (NE) and angiotensin II (AngII) as well as angiotensin II type 1 receptor (AT1) protein expression in the PVN. SHR-ACE2-ExT showed the largest decrease in AngII and AT1 protein expression. Reactive oxygen species (ROS) level and NADPH oxidase (NOX2 and NOX4) protein expression in PVN were also decreased in SHR-ACE2-ExT group than in SHR-ACE2 and SHR-ExT groups. It was concluded that the combined effect has effectively prevented prehypertension progression and baroreflex dysfunction in SHR, which is associated with the reduction in AngII/AT1 axis function and oxidative stress in the PVN.
Angiotensin-converting enzyme 2 (
) gene in combination with exercise training (ExT) delayed the progression of hypertension via normalizing the blunted baroreflex sensitivity (BRS) and inhibiting sympathetic nerve activity (SNA). Its underlying mechanism may be related to the inhibition of AngII/AT1 axis function and central oxidative stress in the paraventricular nucleus (PVN) of prehypertensive rats.</description><subject>ACE2</subject><subject>ACE2 gene</subject><subject>Angiotensin</subject><subject>Angiotensin I - metabolism</subject><subject>Angiotensin II</subject><subject>Angiotensin II - metabolism</subject><subject>Angiotensin-converting enzyme 2</subject><subject>Angiotensin-Converting Enzyme 2 - metabolism</subject><subject>Animal models</subject><subject>Animals</subject><subject>Baroreceptors</subject><subject>Blood Pressure</subject><subject>CYBB protein</subject><subject>Fitness training programs</subject><subject>Fluorescence</subject><subject>Green fluorescent protein</subject><subject>Hypertension</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - therapy</subject><subject>Male</subject><subject>NAD(P)H oxidase</subject><subject>Norepinephrine</subject><subject>NOX4 protein</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - physiology</subject><subject>Paraventricular Hypothalamic Nucleus</subject><subject>Paraventricular nucleus</subject><subject>Peptidyl-dipeptidase A</subject><subject>Physical Conditioning, Animal - physiology</subject><subject>Physical training</subject><subject>Prehypertension - metabolism</subject><subject>Pressure effects</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>Reactive oxygen species</subject><subject>Reflexes</subject><subject>Training</subject><issn>8750-7587</issn><issn>1522-1601</issn><issn>1522-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc9q3DAQh0VJabZpX6ER5NKLN5KsP_ZxWZJmIdBLejayPN7VYkuOJCe7b5DHrjZJSykMDMx882PgQ-iSkiWlgl3v9TQN0-4YrR-WhHBRLxlh9ANa5C0rqCT0DC0qJUihRKXO0ecY94RQzgX9hM5LIbikTC3Qy2p9w_AWHGDjx9Y66PCzTTsMBwjGRsApaOus22KdErhZJ4jYgMvjAa_cdrO5Xj1QrA824n52JlnvsHYd9gfb6WSfAMcUIEZs8xxPAXbHCUKOiqdd0AmPvoPhC_rY6yHC1_d-gX7d3jys74r7nz8269V9YUpOU9FTDpVUdatFRZTq-6oWubQAAqJvFeHEgClL1jJBFWFclW3NJHAudVtLVl6g72-5U_CPM8TUjDYaGAbtwM-xYVJyVfOa04xe_Yfu_Rxc_i5TSshaVqTMlHqjTPAxBuibKdhRh2NDSXOS1fwrq3mV1Zxk5ctv7_lzO0L39-6PnfI3pdyUjw</recordid><startdate>20220601</startdate><enddate>20220601</enddate><creator>Chen, Xiu-Yun</creator><creator>Lin, Cheng</creator><creator>Liu, Guo-Ying</creator><creator>Pei, Chun</creator><creator>Xu, Gui-Qing</creator><creator>Gao, Lie</creator><creator>Wang, Shi-Zhong</creator><creator>Pan, Yan-Xia</creator><general>American Physiological Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-1025-2290</orcidid><orcidid>https://orcid.org/0000-0002-0570-4117</orcidid></search><sort><creationdate>20220601</creationdate><title>ACE2 gene combined with exercise training attenuates central AngII/AT1 axis function and oxidative stress in a prehypertensive rat model</title><author>Chen, Xiu-Yun ; Lin, Cheng ; Liu, Guo-Ying ; Pei, Chun ; Xu, Gui-Qing ; Gao, Lie ; Wang, Shi-Zhong ; Pan, Yan-Xia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c341t-f14e8679ba58077ff895895a5e0e5fb7040cec332b251702473b926e446ab9623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>ACE2</topic><topic>ACE2 gene</topic><topic>Angiotensin</topic><topic>Angiotensin I - metabolism</topic><topic>Angiotensin II</topic><topic>Angiotensin II - metabolism</topic><topic>Angiotensin-converting enzyme 2</topic><topic>Angiotensin-Converting Enzyme 2 - metabolism</topic><topic>Animal models</topic><topic>Animals</topic><topic>Baroreceptors</topic><topic>Blood Pressure</topic><topic>CYBB protein</topic><topic>Fitness training programs</topic><topic>Fluorescence</topic><topic>Green fluorescent protein</topic><topic>Hypertension</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - therapy</topic><topic>Male</topic><topic>NAD(P)H oxidase</topic><topic>Norepinephrine</topic><topic>NOX4 protein</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - physiology</topic><topic>Paraventricular Hypothalamic Nucleus</topic><topic>Paraventricular nucleus</topic><topic>Peptidyl-dipeptidase A</topic><topic>Physical Conditioning, Animal - physiology</topic><topic>Physical training</topic><topic>Prehypertension - metabolism</topic><topic>Pressure effects</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Reactive oxygen species</topic><topic>Reflexes</topic><topic>Training</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Xiu-Yun</creatorcontrib><creatorcontrib>Lin, Cheng</creatorcontrib><creatorcontrib>Liu, Guo-Ying</creatorcontrib><creatorcontrib>Pei, Chun</creatorcontrib><creatorcontrib>Xu, Gui-Qing</creatorcontrib><creatorcontrib>Gao, Lie</creatorcontrib><creatorcontrib>Wang, Shi-Zhong</creatorcontrib><creatorcontrib>Pan, Yan-Xia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of applied physiology (1985)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Xiu-Yun</au><au>Lin, Cheng</au><au>Liu, Guo-Ying</au><au>Pei, Chun</au><au>Xu, Gui-Qing</au><au>Gao, Lie</au><au>Wang, Shi-Zhong</au><au>Pan, Yan-Xia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ACE2 gene combined with exercise training attenuates central AngII/AT1 axis function and oxidative stress in a prehypertensive rat model</atitle><jtitle>Journal of applied physiology (1985)</jtitle><addtitle>J Appl Physiol (1985)</addtitle><date>2022-06-01</date><risdate>2022</risdate><volume>132</volume><issue>6</issue><spage>1460</spage><epage>1467</epage><pages>1460-1467</pages><issn>8750-7587</issn><issn>1522-1601</issn><eissn>1522-1601</eissn><abstract>Angiotensin-converting enzyme 2 (ACE2) or exercise training (ExT) is beneficial to hypertension, but their combined effects remain unknown. In this study, lentivirus containing enhanced green fluorescent protein (eGFP) and
were microinjected into the paraventricular nucleus (PVN) of young male spontaneous hypertensive rats (SHRs), and SHRs were assigned into five groups: sedentary (SHR), SHR-ExT, SHR-eGFP,
gene (SHR-ACE2), and
gene combined with ExT (SHR-ACE2-ExT). Wistar-Kyoto (WKY) rats were used as a control.
gene or ExT significantly delayed the elevation of blood pressure, and the combined effect prevented the development and progression of prehypertension. Either
overexpression or ExT improved arterial baroreflex sensitivity (BRS), whereas the combined effect normalized BRS in SHR. Compared with SHR, SHR-ACE2 and SHR-ExT displayed a significantly higher level of ACE2 protein but had lower plasma norepinephrine (NE) and angiotensin II (AngII) as well as angiotensin II type 1 receptor (AT1) protein expression in the PVN. SHR-ACE2-ExT showed the largest decrease in AngII and AT1 protein expression. Reactive oxygen species (ROS) level and NADPH oxidase (NOX2 and NOX4) protein expression in PVN were also decreased in SHR-ACE2-ExT group than in SHR-ACE2 and SHR-ExT groups. It was concluded that the combined effect has effectively prevented prehypertension progression and baroreflex dysfunction in SHR, which is associated with the reduction in AngII/AT1 axis function and oxidative stress in the PVN.
Angiotensin-converting enzyme 2 (
) gene in combination with exercise training (ExT) delayed the progression of hypertension via normalizing the blunted baroreflex sensitivity (BRS) and inhibiting sympathetic nerve activity (SNA). Its underlying mechanism may be related to the inhibition of AngII/AT1 axis function and central oxidative stress in the paraventricular nucleus (PVN) of prehypertensive rats.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>35546127</pmid><doi>10.1152/japplphysiol.00459.2021</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-1025-2290</orcidid><orcidid>https://orcid.org/0000-0002-0570-4117</orcidid></addata></record> |
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source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
subjects | ACE2 ACE2 gene Angiotensin Angiotensin I - metabolism Angiotensin II Angiotensin II - metabolism Angiotensin-converting enzyme 2 Angiotensin-Converting Enzyme 2 - metabolism Animal models Animals Baroreceptors Blood Pressure CYBB protein Fitness training programs Fluorescence Green fluorescent protein Hypertension Hypertension - metabolism Hypertension - therapy Male NAD(P)H oxidase Norepinephrine NOX4 protein Oxidative stress Oxidative Stress - physiology Paraventricular Hypothalamic Nucleus Paraventricular nucleus Peptidyl-dipeptidase A Physical Conditioning, Animal - physiology Physical training Prehypertension - metabolism Pressure effects Protein expression Proteins Rats Rats, Inbred SHR Rats, Inbred WKY Reactive oxygen species Reflexes Training |
title | ACE2 gene combined with exercise training attenuates central AngII/AT1 axis function and oxidative stress in a prehypertensive rat model |
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