Oxidative status in the macula densa modulates tubuloglomerular feedback responsiveness in Angiotensin II-induced hypertension
Aim Tubuloglomerular feedback (TGF) is an important mechanism in control of signal nephron glomerular filtration rate. The oxidative stress in the macula densa, primarily determined by the interactions between nitric oxide (NO) and superoxide (O2−), is essential in maintaining the TGF responsiveness...
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| Veröffentlicht in: | Acta Physiologica 2015-01, Vol.213 (1), p.249-258 |
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| creator | Song, J. Lu, Y. Lai, E. Y. Wei, J. Wang, L. Chandrashekar, K. Wang, S. Shen, C. Juncos, L. A. Liu, R. |
| description | Aim
Tubuloglomerular feedback (TGF) is an important mechanism in control of signal nephron glomerular filtration rate. The oxidative stress in the macula densa, primarily determined by the interactions between nitric oxide (NO) and superoxide (O2−), is essential in maintaining the TGF responsiveness. However, few studies examining the interactions between and amount of NO and O2− generated by the macula densa during normal and hypertensive states.
Methods
In this study, we used isolated perfused juxtaglomerular apparatus to directly measure the amount and also studied the interactions between NO and O2− in macula densa in both physiological and slow pressor Angiotensin II (Ang II)‐induced hypertensive mice.
Results
We found that slow pressor Ang II at a dose of 600 ng kg−1 min−1 for two weeks increased mean arterial pressure by 26.1 ± 5.7 mmHg. TGF response increased from 3.4 ± 0.2 μm in control to 5.2 ± 0.2 μm in hypertensive mice. We first measured O2− generation by the macula densa and found it was undetectable in control mice. However, O2− generation by the macula densa increased to 21.4 ± 2.5 unit min−1 in Ang II‐induced hypertensive mice. We then measured NO generation and found that NO generation by the macula densa was 138.5 ± 9.3 unit min−1 in control mice. The NO was undetectable in the macula densa in hypertensive mice infused with Ang II.
Conclusions
Under physiological conditions, TGF response is mainly controlled by the NO generated in the macula densa; in Ang II induced hypertension, the TGF response is mainly controlled by the O2− generated by the macula densa. |
| doi_str_mv | 10.1111/apha.12358 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_1636408811</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3527407651</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5018-99a8527a3d6063c6da4efb1372ef0301d5ca3fd6db54c8cc3280b7d1c2f895773</originalsourceid><addsrcrecordid>eNp9kE1P4zAQhi0EAgRc-AErS3tDCuuPJHaPVUWhFVqQdlccLcee0EASB9vZpRd-O6aFHncuMx4981h6ETqn5JKm-qGHlb6kjBdyDx1TkcuMClru72Yij9BZCE-EEMoozxk7REesIHJCSH6M3u5eG6tj8xdwiDqOATc9jivAnTZjq7GFPmjcOZseEQKOYzW27rF1Hfi08rgGsJU2z9hDGFwfkqmHsNFM-8fGxSRI82KRNb0dDVi8Wg_gN2vXn6KDWrcBzj77Cfozv_o9u8lu764Xs-ltZgpCZTaZaFkwobktSclNaXUOdUW5YFATTqgtjOa1LW1V5EYaw5kklbDUsFpOCiH4Cfq-9Q7evYwQonpyo-_Tl4qWvMyJlJQm6mJLGe9C8FCrwTed9mtFifpIW32krTZpJ_jbp3KsOrA79CvbBNAt8K9pYf0flZre30y_pNn2pgkRXnc32j-rUnBRqIef12o5ny_vl79mSvJ3HhObpg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1636408811</pqid></control><display><type>article</type><title>Oxidative status in the macula densa modulates tubuloglomerular feedback responsiveness in Angiotensin II-induced hypertension</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Song, J. ; Lu, Y. ; Lai, E. Y. ; Wei, J. ; Wang, L. ; Chandrashekar, K. ; Wang, S. ; Shen, C. ; Juncos, L. A. ; Liu, R.</creator><creatorcontrib>Song, J. ; Lu, Y. ; Lai, E. Y. ; Wei, J. ; Wang, L. ; Chandrashekar, K. ; Wang, S. ; Shen, C. ; Juncos, L. A. ; Liu, R.</creatorcontrib><description>Aim
Tubuloglomerular feedback (TGF) is an important mechanism in control of signal nephron glomerular filtration rate. The oxidative stress in the macula densa, primarily determined by the interactions between nitric oxide (NO) and superoxide (O2−), is essential in maintaining the TGF responsiveness. However, few studies examining the interactions between and amount of NO and O2− generated by the macula densa during normal and hypertensive states.
Methods
In this study, we used isolated perfused juxtaglomerular apparatus to directly measure the amount and also studied the interactions between NO and O2− in macula densa in both physiological and slow pressor Angiotensin II (Ang II)‐induced hypertensive mice.
Results
We found that slow pressor Ang II at a dose of 600 ng kg−1 min−1 for two weeks increased mean arterial pressure by 26.1 ± 5.7 mmHg. TGF response increased from 3.4 ± 0.2 μm in control to 5.2 ± 0.2 μm in hypertensive mice. We first measured O2− generation by the macula densa and found it was undetectable in control mice. However, O2− generation by the macula densa increased to 21.4 ± 2.5 unit min−1 in Ang II‐induced hypertensive mice. We then measured NO generation and found that NO generation by the macula densa was 138.5 ± 9.3 unit min−1 in control mice. The NO was undetectable in the macula densa in hypertensive mice infused with Ang II.
Conclusions
Under physiological conditions, TGF response is mainly controlled by the NO generated in the macula densa; in Ang II induced hypertension, the TGF response is mainly controlled by the O2− generated by the macula densa.</description><identifier>ISSN: 1748-1708</identifier><identifier>EISSN: 1748-1716</identifier><identifier>DOI: 10.1111/apha.12358</identifier><identifier>PMID: 25089004</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Angiotensin II - pharmacology ; Animals ; Blood Pressure - drug effects ; Blood Pressure - physiology ; Disease Models, Animal ; hypertension ; Hypertension - chemically induced ; Hypertension - metabolism ; Kidney Glomerulus - drug effects ; Kidney Glomerulus - metabolism ; Kidney Tubules - drug effects ; macula densa ; Mice, Inbred C57BL ; Nephrons - drug effects ; Nephrons - metabolism ; Nitric Oxide - metabolism ; Oxidative Stress ; tubuloglomerular feedback ; Vasoconstrictor Agents - pharmacology</subject><ispartof>Acta Physiologica, 2015-01, Vol.213 (1), p.249-258</ispartof><rights>2014 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd</rights><rights>2014 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.</rights><rights>Copyright © 2015 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5018-99a8527a3d6063c6da4efb1372ef0301d5ca3fd6db54c8cc3280b7d1c2f895773</citedby><cites>FETCH-LOGICAL-c5018-99a8527a3d6063c6da4efb1372ef0301d5ca3fd6db54c8cc3280b7d1c2f895773</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fapha.12358$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fapha.12358$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25089004$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Song, J.</creatorcontrib><creatorcontrib>Lu, Y.</creatorcontrib><creatorcontrib>Lai, E. Y.</creatorcontrib><creatorcontrib>Wei, J.</creatorcontrib><creatorcontrib>Wang, L.</creatorcontrib><creatorcontrib>Chandrashekar, K.</creatorcontrib><creatorcontrib>Wang, S.</creatorcontrib><creatorcontrib>Shen, C.</creatorcontrib><creatorcontrib>Juncos, L. A.</creatorcontrib><creatorcontrib>Liu, R.</creatorcontrib><title>Oxidative status in the macula densa modulates tubuloglomerular feedback responsiveness in Angiotensin II-induced hypertension</title><title>Acta Physiologica</title><addtitle>Acta Physiol</addtitle><description>Aim
Tubuloglomerular feedback (TGF) is an important mechanism in control of signal nephron glomerular filtration rate. The oxidative stress in the macula densa, primarily determined by the interactions between nitric oxide (NO) and superoxide (O2−), is essential in maintaining the TGF responsiveness. However, few studies examining the interactions between and amount of NO and O2− generated by the macula densa during normal and hypertensive states.
Methods
In this study, we used isolated perfused juxtaglomerular apparatus to directly measure the amount and also studied the interactions between NO and O2− in macula densa in both physiological and slow pressor Angiotensin II (Ang II)‐induced hypertensive mice.
Results
We found that slow pressor Ang II at a dose of 600 ng kg−1 min−1 for two weeks increased mean arterial pressure by 26.1 ± 5.7 mmHg. TGF response increased from 3.4 ± 0.2 μm in control to 5.2 ± 0.2 μm in hypertensive mice. We first measured O2− generation by the macula densa and found it was undetectable in control mice. However, O2− generation by the macula densa increased to 21.4 ± 2.5 unit min−1 in Ang II‐induced hypertensive mice. We then measured NO generation and found that NO generation by the macula densa was 138.5 ± 9.3 unit min−1 in control mice. The NO was undetectable in the macula densa in hypertensive mice infused with Ang II.
Conclusions
Under physiological conditions, TGF response is mainly controlled by the NO generated in the macula densa; in Ang II induced hypertension, the TGF response is mainly controlled by the O2− generated by the macula densa.</description><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Disease Models, Animal</subject><subject>hypertension</subject><subject>Hypertension - chemically induced</subject><subject>Hypertension - metabolism</subject><subject>Kidney Glomerulus - drug effects</subject><subject>Kidney Glomerulus - metabolism</subject><subject>Kidney Tubules - drug effects</subject><subject>macula densa</subject><subject>Mice, Inbred C57BL</subject><subject>Nephrons - drug effects</subject><subject>Nephrons - metabolism</subject><subject>Nitric Oxide - metabolism</subject><subject>Oxidative Stress</subject><subject>tubuloglomerular feedback</subject><subject>Vasoconstrictor Agents - pharmacology</subject><issn>1748-1708</issn><issn>1748-1716</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1P4zAQhi0EAgRc-AErS3tDCuuPJHaPVUWhFVqQdlccLcee0EASB9vZpRd-O6aFHncuMx4981h6ETqn5JKm-qGHlb6kjBdyDx1TkcuMClru72Yij9BZCE-EEMoozxk7REesIHJCSH6M3u5eG6tj8xdwiDqOATc9jivAnTZjq7GFPmjcOZseEQKOYzW27rF1Hfi08rgGsJU2z9hDGFwfkqmHsNFM-8fGxSRI82KRNb0dDVi8Wg_gN2vXn6KDWrcBzj77Cfozv_o9u8lu764Xs-ltZgpCZTaZaFkwobktSclNaXUOdUW5YFATTqgtjOa1LW1V5EYaw5kklbDUsFpOCiH4Cfq-9Q7evYwQonpyo-_Tl4qWvMyJlJQm6mJLGe9C8FCrwTed9mtFifpIW32krTZpJ_jbp3KsOrA79CvbBNAt8K9pYf0flZre30y_pNn2pgkRXnc32j-rUnBRqIef12o5ny_vl79mSvJ3HhObpg</recordid><startdate>201501</startdate><enddate>201501</enddate><creator>Song, J.</creator><creator>Lu, Y.</creator><creator>Lai, E. Y.</creator><creator>Wei, J.</creator><creator>Wang, L.</creator><creator>Chandrashekar, K.</creator><creator>Wang, S.</creator><creator>Shen, C.</creator><creator>Juncos, L. A.</creator><creator>Liu, R.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7TK</scope><scope>7TS</scope></search><sort><creationdate>201501</creationdate><title>Oxidative status in the macula densa modulates tubuloglomerular feedback responsiveness in Angiotensin II-induced hypertension</title><author>Song, J. ; Lu, Y. ; Lai, E. Y. ; Wei, J. ; Wang, L. ; Chandrashekar, K. ; Wang, S. ; Shen, C. ; Juncos, L. A. ; Liu, R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5018-99a8527a3d6063c6da4efb1372ef0301d5ca3fd6db54c8cc3280b7d1c2f895773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Pressure - physiology</topic><topic>Disease Models, Animal</topic><topic>hypertension</topic><topic>Hypertension - chemically induced</topic><topic>Hypertension - metabolism</topic><topic>Kidney Glomerulus - drug effects</topic><topic>Kidney Glomerulus - metabolism</topic><topic>Kidney Tubules - drug effects</topic><topic>macula densa</topic><topic>Mice, Inbred C57BL</topic><topic>Nephrons - drug effects</topic><topic>Nephrons - metabolism</topic><topic>Nitric Oxide - metabolism</topic><topic>Oxidative Stress</topic><topic>tubuloglomerular feedback</topic><topic>Vasoconstrictor Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Song, J.</creatorcontrib><creatorcontrib>Lu, Y.</creatorcontrib><creatorcontrib>Lai, E. Y.</creatorcontrib><creatorcontrib>Wei, J.</creatorcontrib><creatorcontrib>Wang, L.</creatorcontrib><creatorcontrib>Chandrashekar, K.</creatorcontrib><creatorcontrib>Wang, S.</creatorcontrib><creatorcontrib>Shen, C.</creatorcontrib><creatorcontrib>Juncos, L. A.</creatorcontrib><creatorcontrib>Liu, R.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><jtitle>Acta Physiologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Song, J.</au><au>Lu, Y.</au><au>Lai, E. Y.</au><au>Wei, J.</au><au>Wang, L.</au><au>Chandrashekar, K.</au><au>Wang, S.</au><au>Shen, C.</au><au>Juncos, L. A.</au><au>Liu, R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative status in the macula densa modulates tubuloglomerular feedback responsiveness in Angiotensin II-induced hypertension</atitle><jtitle>Acta Physiologica</jtitle><addtitle>Acta Physiol</addtitle><date>2015-01</date><risdate>2015</risdate><volume>213</volume><issue>1</issue><spage>249</spage><epage>258</epage><pages>249-258</pages><issn>1748-1708</issn><eissn>1748-1716</eissn><abstract>Aim
Tubuloglomerular feedback (TGF) is an important mechanism in control of signal nephron glomerular filtration rate. The oxidative stress in the macula densa, primarily determined by the interactions between nitric oxide (NO) and superoxide (O2−), is essential in maintaining the TGF responsiveness. However, few studies examining the interactions between and amount of NO and O2− generated by the macula densa during normal and hypertensive states.
Methods
In this study, we used isolated perfused juxtaglomerular apparatus to directly measure the amount and also studied the interactions between NO and O2− in macula densa in both physiological and slow pressor Angiotensin II (Ang II)‐induced hypertensive mice.
Results
We found that slow pressor Ang II at a dose of 600 ng kg−1 min−1 for two weeks increased mean arterial pressure by 26.1 ± 5.7 mmHg. TGF response increased from 3.4 ± 0.2 μm in control to 5.2 ± 0.2 μm in hypertensive mice. We first measured O2− generation by the macula densa and found it was undetectable in control mice. However, O2− generation by the macula densa increased to 21.4 ± 2.5 unit min−1 in Ang II‐induced hypertensive mice. We then measured NO generation and found that NO generation by the macula densa was 138.5 ± 9.3 unit min−1 in control mice. The NO was undetectable in the macula densa in hypertensive mice infused with Ang II.
Conclusions
Under physiological conditions, TGF response is mainly controlled by the NO generated in the macula densa; in Ang II induced hypertension, the TGF response is mainly controlled by the O2− generated by the macula densa.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>25089004</pmid><doi>10.1111/apha.12358</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiotensin II - pharmacology Animals Blood Pressure - drug effects Blood Pressure - physiology Disease Models, Animal hypertension Hypertension - chemically induced Hypertension - metabolism Kidney Glomerulus - drug effects Kidney Glomerulus - metabolism Kidney Tubules - drug effects macula densa Mice, Inbred C57BL Nephrons - drug effects Nephrons - metabolism Nitric Oxide - metabolism Oxidative Stress tubuloglomerular feedback Vasoconstrictor Agents - pharmacology |
| title | Oxidative status in the macula densa modulates tubuloglomerular feedback responsiveness in Angiotensin II-induced hypertension |
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