Effect of baroreflex activation therapy on renal sodium excretion in patients with resistant hypertension
Objective Activation of the sympathetic nervous system increases sodium retention in resistant hypertension. Baroreflex activation therapy (BAT) is an interventional method to reduce sympathetic overactivity in patients with resistant hypertension. This study aimed to assess the effect of BAT on uri...
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| Veröffentlicht in: | Clinical research in cardiology 2019-11, Vol.108 (11), p.1287-1296 |
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| creator | Lipphardt, Mark Koziolek, Michael J. Lehnig, Luca-Yves Schäfer, Ann-Kathrin Müller, Gerhard A. Lüders, Stephan Wallbach, Manuel |
| description | Objective
Activation of the sympathetic nervous system increases sodium retention in resistant hypertension. Baroreflex activation therapy (BAT) is an interventional method to reduce sympathetic overactivity in patients with resistant hypertension. This study aimed to assess the effect of BAT on urinary sodium excretion.
Methods
From 2012 to 2015, consecutive patients with resistant hypertension and blood pressure (BP) above target despite polypharmacy strategies were consecutively included in this observational study. BAT was provided with the individual adaption of programmed parameters over the first months. 24-h urinary sodium excretion (UNa) was estimated at baseline and after 6 months using the Kawasaki formula in patients undergoing BAT. Additionally, the fractional sodium excretion, plasma renin activity, and aldosterone levels were assessed.
Results
Forty-two patients completed the 6-month follow-up period. Office systolic and ambulatory 24-h systolic BP at baseline were 169 ± 27 mmHg and 148 ± 16 mmHg despite a median intake of 7(3–9) antihypertensive drugs. After 6 months of BAT, systolic office BP decreased to 150 ± 29 mmHg (
p
|
| doi_str_mv | 10.1007/s00392-019-01464-4 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2205412999</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2205412999</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-416a8c7077ef09f900e6b8b0e4b32028bce21861857e33074a167021f63efe7b3</originalsourceid><addsrcrecordid>eNp9kctKxTAQhoMo3l_AhQTcuKlOLm2apYg3ENzoOqR14on0tDVJ1fP2xnO8gAsXwwzkm38y8xNywOCEAajTCCA0L4DpHLKShVwj26yuWAGV5us_dS23yE6MzwAlAyE3yZYAXZag1DbxF85hm-jgaGPDENB1-E5tm_yrTX7oaZphsOOC5jJgbzsah0c_zSm-twGXhO_pmFnsU6RvPs0yF31Mtk90thgxJOxj5vbIhrNdxP2vvEseLi_uz6-L27urm_Oz26IVqkyFZJWtW5U_hw600wBYNXUDKBvBgddNi_xzr7pUKAQoaVmlgDNXCXSoGrFLjle6YxheJozJzH1ssetsj8MUDedQSsa11hk9-oM-D1PISy4pCbJkZZ0pvqLaMMSYL2TG4Oc2LAwD82mEWRlhshFmaYSRuenwS3pq5vj40_J9-QyIFRDzU_-E4Xf2P7IfebKT5A</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2204045158</pqid></control><display><type>article</type><title>Effect of baroreflex activation therapy on renal sodium excretion in patients with resistant hypertension</title><source>MEDLINE</source><source>Springer Journals</source><creator>Lipphardt, Mark ; Koziolek, Michael J. ; Lehnig, Luca-Yves ; Schäfer, Ann-Kathrin ; Müller, Gerhard A. ; Lüders, Stephan ; Wallbach, Manuel</creator><creatorcontrib>Lipphardt, Mark ; Koziolek, Michael J. ; Lehnig, Luca-Yves ; Schäfer, Ann-Kathrin ; Müller, Gerhard A. ; Lüders, Stephan ; Wallbach, Manuel</creatorcontrib><description>Objective
Activation of the sympathetic nervous system increases sodium retention in resistant hypertension. Baroreflex activation therapy (BAT) is an interventional method to reduce sympathetic overactivity in patients with resistant hypertension. This study aimed to assess the effect of BAT on urinary sodium excretion.
Methods
From 2012 to 2015, consecutive patients with resistant hypertension and blood pressure (BP) above target despite polypharmacy strategies were consecutively included in this observational study. BAT was provided with the individual adaption of programmed parameters over the first months. 24-h urinary sodium excretion (UNa) was estimated at baseline and after 6 months using the Kawasaki formula in patients undergoing BAT. Additionally, the fractional sodium excretion, plasma renin activity, and aldosterone levels were assessed.
Results
Forty-two patients completed the 6-month follow-up period. Office systolic and ambulatory 24-h systolic BP at baseline were 169 ± 27 mmHg and 148 ± 16 mmHg despite a median intake of 7(3–9) antihypertensive drugs. After 6 months of BAT, systolic office BP decreased to 150 ± 29 mmHg (
p
< 0.01), 24-h systolic BP to 142 ± 22 mmHg (
p
= 0.04) and 24-h UNa increased by 37% compared to baseline (128 ± 66 vs. 155 ± 83 mmol/day,
p
< 0.01). These findings were accompanied by a significant increase in fractional sodium excretion (0.74% [0.43–1.47] to 0.92% [0.61–1.92];
p
= 0.02). However, in contrast to the significant BP reduction, eGFR, plasma sodium, renin activity and aldosterone levels did not change during BAT. The increase in sodium excretion was correlated with the change in eGFR (
r
= 0.371;
p
= 0.015).
Conclusion
The present study revealed a significant increase of estimated 24-h UNa which may contribute to the long-term BP-lowering effects of this interventional method.</description><identifier>ISSN: 1861-0684</identifier><identifier>EISSN: 1861-0692</identifier><identifier>DOI: 10.1007/s00392-019-01464-4</identifier><identifier>PMID: 30955077</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Activation ; Adult ; Aged ; Aldosterone ; Antihypertensive Agents - therapeutic use ; Antihypertensives ; Baroreceptors ; Baroreflex - physiology ; Blood pressure ; Cardiology ; Cohort Studies ; Epidermal growth factor receptors ; Excretion ; Female ; Glomerular Filtration Rate ; Humans ; Hypertension ; Hypertension - complications ; Hypertension - physiopathology ; Hypertension - therapy ; Kidney - metabolism ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Original Paper ; Patients ; Reflexes ; Renal function ; Renin ; Sodium ; Sodium - urine ; Sympathetic nervous system ; Therapy ; Treatment Outcome</subject><ispartof>Clinical research in cardiology, 2019-11, Vol.108 (11), p.1287-1296</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2019</rights><rights>Clinical Research in Cardiology is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-416a8c7077ef09f900e6b8b0e4b32028bce21861857e33074a167021f63efe7b3</citedby><cites>FETCH-LOGICAL-c375t-416a8c7077ef09f900e6b8b0e4b32028bce21861857e33074a167021f63efe7b3</cites><orcidid>0000-0002-1162-4682</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00392-019-01464-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00392-019-01464-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30955077$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lipphardt, Mark</creatorcontrib><creatorcontrib>Koziolek, Michael J.</creatorcontrib><creatorcontrib>Lehnig, Luca-Yves</creatorcontrib><creatorcontrib>Schäfer, Ann-Kathrin</creatorcontrib><creatorcontrib>Müller, Gerhard A.</creatorcontrib><creatorcontrib>Lüders, Stephan</creatorcontrib><creatorcontrib>Wallbach, Manuel</creatorcontrib><title>Effect of baroreflex activation therapy on renal sodium excretion in patients with resistant hypertension</title><title>Clinical research in cardiology</title><addtitle>Clin Res Cardiol</addtitle><addtitle>Clin Res Cardiol</addtitle><description>Objective
Activation of the sympathetic nervous system increases sodium retention in resistant hypertension. Baroreflex activation therapy (BAT) is an interventional method to reduce sympathetic overactivity in patients with resistant hypertension. This study aimed to assess the effect of BAT on urinary sodium excretion.
Methods
From 2012 to 2015, consecutive patients with resistant hypertension and blood pressure (BP) above target despite polypharmacy strategies were consecutively included in this observational study. BAT was provided with the individual adaption of programmed parameters over the first months. 24-h urinary sodium excretion (UNa) was estimated at baseline and after 6 months using the Kawasaki formula in patients undergoing BAT. Additionally, the fractional sodium excretion, plasma renin activity, and aldosterone levels were assessed.
Results
Forty-two patients completed the 6-month follow-up period. Office systolic and ambulatory 24-h systolic BP at baseline were 169 ± 27 mmHg and 148 ± 16 mmHg despite a median intake of 7(3–9) antihypertensive drugs. After 6 months of BAT, systolic office BP decreased to 150 ± 29 mmHg (
p
< 0.01), 24-h systolic BP to 142 ± 22 mmHg (
p
= 0.04) and 24-h UNa increased by 37% compared to baseline (128 ± 66 vs. 155 ± 83 mmol/day,
p
< 0.01). These findings were accompanied by a significant increase in fractional sodium excretion (0.74% [0.43–1.47] to 0.92% [0.61–1.92];
p
= 0.02). However, in contrast to the significant BP reduction, eGFR, plasma sodium, renin activity and aldosterone levels did not change during BAT. The increase in sodium excretion was correlated with the change in eGFR (
r
= 0.371;
p
= 0.015).
Conclusion
The present study revealed a significant increase of estimated 24-h UNa which may contribute to the long-term BP-lowering effects of this interventional method.</description><subject>Activation</subject><subject>Adult</subject><subject>Aged</subject><subject>Aldosterone</subject><subject>Antihypertensive Agents - therapeutic use</subject><subject>Antihypertensives</subject><subject>Baroreceptors</subject><subject>Baroreflex - physiology</subject><subject>Blood pressure</subject><subject>Cardiology</subject><subject>Cohort Studies</subject><subject>Epidermal growth factor receptors</subject><subject>Excretion</subject><subject>Female</subject><subject>Glomerular Filtration Rate</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension - complications</subject><subject>Hypertension - physiopathology</subject><subject>Hypertension - therapy</subject><subject>Kidney - metabolism</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Original Paper</subject><subject>Patients</subject><subject>Reflexes</subject><subject>Renal function</subject><subject>Renin</subject><subject>Sodium</subject><subject>Sodium - urine</subject><subject>Sympathetic nervous system</subject><subject>Therapy</subject><subject>Treatment Outcome</subject><issn>1861-0684</issn><issn>1861-0692</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kctKxTAQhoMo3l_AhQTcuKlOLm2apYg3ENzoOqR14on0tDVJ1fP2xnO8gAsXwwzkm38y8xNywOCEAajTCCA0L4DpHLKShVwj26yuWAGV5us_dS23yE6MzwAlAyE3yZYAXZag1DbxF85hm-jgaGPDENB1-E5tm_yrTX7oaZphsOOC5jJgbzsah0c_zSm-twGXhO_pmFnsU6RvPs0yF31Mtk90thgxJOxj5vbIhrNdxP2vvEseLi_uz6-L27urm_Oz26IVqkyFZJWtW5U_hw600wBYNXUDKBvBgddNi_xzr7pUKAQoaVmlgDNXCXSoGrFLjle6YxheJozJzH1ssetsj8MUDedQSsa11hk9-oM-D1PISy4pCbJkZZ0pvqLaMMSYL2TG4Oc2LAwD82mEWRlhshFmaYSRuenwS3pq5vj40_J9-QyIFRDzU_-E4Xf2P7IfebKT5A</recordid><startdate>20191101</startdate><enddate>20191101</enddate><creator>Lipphardt, Mark</creator><creator>Koziolek, Michael J.</creator><creator>Lehnig, Luca-Yves</creator><creator>Schäfer, Ann-Kathrin</creator><creator>Müller, Gerhard A.</creator><creator>Lüders, Stephan</creator><creator>Wallbach, Manuel</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7Z</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-1162-4682</orcidid></search><sort><creationdate>20191101</creationdate><title>Effect of baroreflex activation therapy on renal sodium excretion in patients with resistant hypertension</title><author>Lipphardt, Mark ; Koziolek, Michael J. ; Lehnig, Luca-Yves ; Schäfer, Ann-Kathrin ; Müller, Gerhard A. ; Lüders, Stephan ; Wallbach, Manuel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-416a8c7077ef09f900e6b8b0e4b32028bce21861857e33074a167021f63efe7b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Activation</topic><topic>Adult</topic><topic>Aged</topic><topic>Aldosterone</topic><topic>Antihypertensive Agents - therapeutic use</topic><topic>Antihypertensives</topic><topic>Baroreceptors</topic><topic>Baroreflex - physiology</topic><topic>Blood pressure</topic><topic>Cardiology</topic><topic>Cohort Studies</topic><topic>Epidermal growth factor receptors</topic><topic>Excretion</topic><topic>Female</topic><topic>Glomerular Filtration Rate</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension - complications</topic><topic>Hypertension - physiopathology</topic><topic>Hypertension - therapy</topic><topic>Kidney - metabolism</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Original Paper</topic><topic>Patients</topic><topic>Reflexes</topic><topic>Renal function</topic><topic>Renin</topic><topic>Sodium</topic><topic>Sodium - urine</topic><topic>Sympathetic nervous system</topic><topic>Therapy</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lipphardt, Mark</creatorcontrib><creatorcontrib>Koziolek, Michael J.</creatorcontrib><creatorcontrib>Lehnig, Luca-Yves</creatorcontrib><creatorcontrib>Schäfer, Ann-Kathrin</creatorcontrib><creatorcontrib>Müller, Gerhard A.</creatorcontrib><creatorcontrib>Lüders, Stephan</creatorcontrib><creatorcontrib>Wallbach, Manuel</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical research in cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lipphardt, Mark</au><au>Koziolek, Michael J.</au><au>Lehnig, Luca-Yves</au><au>Schäfer, Ann-Kathrin</au><au>Müller, Gerhard A.</au><au>Lüders, Stephan</au><au>Wallbach, Manuel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of baroreflex activation therapy on renal sodium excretion in patients with resistant hypertension</atitle><jtitle>Clinical research in cardiology</jtitle><stitle>Clin Res Cardiol</stitle><addtitle>Clin Res Cardiol</addtitle><date>2019-11-01</date><risdate>2019</risdate><volume>108</volume><issue>11</issue><spage>1287</spage><epage>1296</epage><pages>1287-1296</pages><issn>1861-0684</issn><eissn>1861-0692</eissn><abstract>Objective
Activation of the sympathetic nervous system increases sodium retention in resistant hypertension. Baroreflex activation therapy (BAT) is an interventional method to reduce sympathetic overactivity in patients with resistant hypertension. This study aimed to assess the effect of BAT on urinary sodium excretion.
Methods
From 2012 to 2015, consecutive patients with resistant hypertension and blood pressure (BP) above target despite polypharmacy strategies were consecutively included in this observational study. BAT was provided with the individual adaption of programmed parameters over the first months. 24-h urinary sodium excretion (UNa) was estimated at baseline and after 6 months using the Kawasaki formula in patients undergoing BAT. Additionally, the fractional sodium excretion, plasma renin activity, and aldosterone levels were assessed.
Results
Forty-two patients completed the 6-month follow-up period. Office systolic and ambulatory 24-h systolic BP at baseline were 169 ± 27 mmHg and 148 ± 16 mmHg despite a median intake of 7(3–9) antihypertensive drugs. After 6 months of BAT, systolic office BP decreased to 150 ± 29 mmHg (
p
< 0.01), 24-h systolic BP to 142 ± 22 mmHg (
p
= 0.04) and 24-h UNa increased by 37% compared to baseline (128 ± 66 vs. 155 ± 83 mmol/day,
p
< 0.01). These findings were accompanied by a significant increase in fractional sodium excretion (0.74% [0.43–1.47] to 0.92% [0.61–1.92];
p
= 0.02). However, in contrast to the significant BP reduction, eGFR, plasma sodium, renin activity and aldosterone levels did not change during BAT. The increase in sodium excretion was correlated with the change in eGFR (
r
= 0.371;
p
= 0.015).
Conclusion
The present study revealed a significant increase of estimated 24-h UNa which may contribute to the long-term BP-lowering effects of this interventional method.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>30955077</pmid><doi>10.1007/s00392-019-01464-4</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-1162-4682</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1861-0684 |
| ispartof | Clinical research in cardiology, 2019-11, Vol.108 (11), p.1287-1296 |
| issn | 1861-0684 1861-0692 |
| language | eng |
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| source | MEDLINE; Springer Journals |
| subjects | Activation Adult Aged Aldosterone Antihypertensive Agents - therapeutic use Antihypertensives Baroreceptors Baroreflex - physiology Blood pressure Cardiology Cohort Studies Epidermal growth factor receptors Excretion Female Glomerular Filtration Rate Humans Hypertension Hypertension - complications Hypertension - physiopathology Hypertension - therapy Kidney - metabolism Male Medicine Medicine & Public Health Middle Aged Original Paper Patients Reflexes Renal function Renin Sodium Sodium - urine Sympathetic nervous system Therapy Treatment Outcome |
| title | Effect of baroreflex activation therapy on renal sodium excretion in patients with resistant hypertension |
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