Enhanced Adipose Afferent Reflex Contributes to Sympathetic Activation in Diet-Induced Obesity Hypertension
We recently found that adipose afferent reflex (AAR) induced by chemical stimulation of white adipose tissue (WAT) increased sympathetic outflow and blood pressure in normal rats. The study was designed to test the hypothesis that AAR contributes to sympathetic activation in obesity hypertension. Ma...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2012-11, Vol.60 (5), p.1280-1286 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Xiong, Xiao-Qing Chen, Wei-Wei Han, Ying Zhou, Ye-Bo Zhang, Feng Gao, Xing-Ya Zhu, Guo-Qing |
| description | We recently found that adipose afferent reflex (AAR) induced by chemical stimulation of white adipose tissue (WAT) increased sympathetic outflow and blood pressure in normal rats. The study was designed to test the hypothesis that AAR contributes to sympathetic activation in obesity hypertension. Male rats were fed with a control diet (12% kcal as fat) or high-fat diet (42% kcal as fat) for 12 weeks to induce obesity hypertension. Stimulation of WAT with capsaicin increased renal sympathetic nerve activity and mean arterial pressure. Both AAR and WAT afferent activity were enhanced in obesity hypertension (OH) compared with obesity nonhypertension (ON) and in ON compared with obesity-resistant or control diet rats. WAT sensory denervation induced by resiniferatoxin caused greater decreases in renal sympathetic nerve activity and mean arterial pressure in OH than ON and in ON than obesity-resistant or control. The depressor effect of resiniferatoxin lasted ≥3 weeks in OH. Leptin antagonist in WAT reduced renal sympathetic nerve activity and mean arterial pressure in OH. WAT injection of capsaicin increased plasma renin, angiotensin II, and norepinephrine levels in OH and caused more c-fos expression in paraventricular nucleus in OH than ON and in ON than obesity-resistant or control rats. Inhibiting paraventricular nucleus neurons with lidocaine attenuated renal sympathetic nerve activity in OH and ON, decreased mean arterial pressure in OH, and abolished the capsaicin-induced AAR in all groups. The results indicate that enhanced AAR contributes to sympathetic activation in OH, and paraventricular nucleus plays an important role in the enhanced AAR and sympathetic activation in OH. |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.112.198002 |
| format | Article |
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The study was designed to test the hypothesis that AAR contributes to sympathetic activation in obesity hypertension. Male rats were fed with a control diet (12% kcal as fat) or high-fat diet (42% kcal as fat) for 12 weeks to induce obesity hypertension. Stimulation of WAT with capsaicin increased renal sympathetic nerve activity and mean arterial pressure. Both AAR and WAT afferent activity were enhanced in obesity hypertension (OH) compared with obesity nonhypertension (ON) and in ON compared with obesity-resistant or control diet rats. WAT sensory denervation induced by resiniferatoxin caused greater decreases in renal sympathetic nerve activity and mean arterial pressure in OH than ON and in ON than obesity-resistant or control. The depressor effect of resiniferatoxin lasted ≥3 weeks in OH. Leptin antagonist in WAT reduced renal sympathetic nerve activity and mean arterial pressure in OH. WAT injection of capsaicin increased plasma renin, angiotensin II, and norepinephrine levels in OH and caused more c-fos expression in paraventricular nucleus in OH than ON and in ON than obesity-resistant or control rats. Inhibiting paraventricular nucleus neurons with lidocaine attenuated renal sympathetic nerve activity in OH and ON, decreased mean arterial pressure in OH, and abolished the capsaicin-induced AAR in all groups. The results indicate that enhanced AAR contributes to sympathetic activation in OH, and paraventricular nucleus plays an important role in the enhanced AAR and sympathetic activation in OH.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.112.198002</identifier><identifier>PMID: 23033372</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Adipose Tissue, White - drug effects ; Adipose Tissue, White - innervation ; Adipose Tissue, White - physiopathology ; Angiotensin II - blood ; Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure - drug effects ; Blood Pressure - physiology ; Capsaicin - pharmacology ; Cardiology. Vascular system ; Diet, High-Fat - adverse effects ; Diterpenes - pharmacology ; Enzyme-Linked Immunosorbent Assay ; Hypertension - blood ; Hypertension - etiology ; Hypertension - physiopathology ; Immunohistochemistry ; Lidocaine - pharmacology ; Male ; Medical sciences ; Metabolic diseases ; Norepinephrine - blood ; Obesity ; Obesity - etiology ; Obesity - physiopathology ; Paraventricular Hypothalamic Nucleus - drug effects ; Paraventricular Hypothalamic Nucleus - metabolism ; Proto-Oncogene Proteins c-fos - metabolism ; Rats ; Rats, Sprague-Dawley ; Reflex - physiology ; Renin - blood ; Sensory System Agents - pharmacology ; Sympathetic Nervous System - physiopathology</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2012-11, Vol.60 (5), p.1280-1286</ispartof><rights>2012 American Heart Association, Inc.</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5132-d7c4aa3aae7445547b72ed0384d73bafe31017d3804f312c99eabb2a42d292333</citedby><cites>FETCH-LOGICAL-c5132-d7c4aa3aae7445547b72ed0384d73bafe31017d3804f312c99eabb2a42d292333</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3685,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26494351$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23033372$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiong, Xiao-Qing</creatorcontrib><creatorcontrib>Chen, Wei-Wei</creatorcontrib><creatorcontrib>Han, Ying</creatorcontrib><creatorcontrib>Zhou, Ye-Bo</creatorcontrib><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Gao, Xing-Ya</creatorcontrib><creatorcontrib>Zhu, Guo-Qing</creatorcontrib><title>Enhanced Adipose Afferent Reflex Contributes to Sympathetic Activation in Diet-Induced Obesity Hypertension</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>We recently found that adipose afferent reflex (AAR) induced by chemical stimulation of white adipose tissue (WAT) increased sympathetic outflow and blood pressure in normal rats. The study was designed to test the hypothesis that AAR contributes to sympathetic activation in obesity hypertension. Male rats were fed with a control diet (12% kcal as fat) or high-fat diet (42% kcal as fat) for 12 weeks to induce obesity hypertension. Stimulation of WAT with capsaicin increased renal sympathetic nerve activity and mean arterial pressure. Both AAR and WAT afferent activity were enhanced in obesity hypertension (OH) compared with obesity nonhypertension (ON) and in ON compared with obesity-resistant or control diet rats. WAT sensory denervation induced by resiniferatoxin caused greater decreases in renal sympathetic nerve activity and mean arterial pressure in OH than ON and in ON than obesity-resistant or control. The depressor effect of resiniferatoxin lasted ≥3 weeks in OH. Leptin antagonist in WAT reduced renal sympathetic nerve activity and mean arterial pressure in OH. WAT injection of capsaicin increased plasma renin, angiotensin II, and norepinephrine levels in OH and caused more c-fos expression in paraventricular nucleus in OH than ON and in ON than obesity-resistant or control rats. Inhibiting paraventricular nucleus neurons with lidocaine attenuated renal sympathetic nerve activity in OH and ON, decreased mean arterial pressure in OH, and abolished the capsaicin-induced AAR in all groups. The results indicate that enhanced AAR contributes to sympathetic activation in OH, and paraventricular nucleus plays an important role in the enhanced AAR and sympathetic activation in OH.</description><subject>Adipose Tissue, White - drug effects</subject><subject>Adipose Tissue, White - innervation</subject><subject>Adipose Tissue, White - physiopathology</subject><subject>Angiotensin II - blood</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Capsaicin - pharmacology</subject><subject>Cardiology. Vascular system</subject><subject>Diet, High-Fat - adverse effects</subject><subject>Diterpenes - pharmacology</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Hypertension - blood</subject><subject>Hypertension - etiology</subject><subject>Hypertension - physiopathology</subject><subject>Immunohistochemistry</subject><subject>Lidocaine - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Norepinephrine - blood</subject><subject>Obesity</subject><subject>Obesity - etiology</subject><subject>Obesity - physiopathology</subject><subject>Paraventricular Hypothalamic Nucleus - drug effects</subject><subject>Paraventricular Hypothalamic Nucleus - metabolism</subject><subject>Proto-Oncogene Proteins c-fos - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reflex - physiology</subject><subject>Renin - blood</subject><subject>Sensory System Agents - pharmacology</subject><subject>Sympathetic Nervous System - physiopathology</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkN-LEzEQx4MoXq33L0gQBF_2zCTZbtcHYanVFo6r3A_QpyWbzNJ42-xekvXsf2-O1jvwyaeB4TPfmfkQ8hbYGcAMPqx-fFteXi8vrtabi2pVpSY_g3LOGH9GJpBzmcl8Jp6TCYNSZiXA9xPyKoSfjIGUsnhJTrhgQoiCT8jt0m2V02hoZezQB6RV26JHF-klth3-poveRW-bMWKgsadX-92g4haj1bTS0f5S0faOWkc_W4zZ2pnxIW3TYLBxT1f7AX1EFxL0mrxoVRfw9Fin5ObL8nqxys43X9eL6jzTOQiemUJLpYRSWEiZ57JoCo6Gibk0hWhUiwIYFEbMmWwFcF2WqJqGK8kNL3n6a0reH3IH39-NGGK9s0Fj1ymH_RhqABDlPKXwhH48oNr3IXhs68HbnfL7Glj9ILv-R3Zq8vogOw2_Oe4Zmx2ax9G_dhPw7giooFXX-mTahiduJksp0s9T8unA3fddRB9uu_Eefb1F1cXt_1zyB2NHnmY</recordid><startdate>201211</startdate><enddate>201211</enddate><creator>Xiong, Xiao-Qing</creator><creator>Chen, Wei-Wei</creator><creator>Han, Ying</creator><creator>Zhou, Ye-Bo</creator><creator>Zhang, Feng</creator><creator>Gao, Xing-Ya</creator><creator>Zhu, Guo-Qing</creator><general>American Heart Association, Inc</general><general>Lippincott Williams & Wilkins</general><scope>IQODW</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>7X8</scope></search><sort><creationdate>201211</creationdate><title>Enhanced Adipose Afferent Reflex Contributes to Sympathetic Activation in Diet-Induced Obesity Hypertension</title><author>Xiong, Xiao-Qing ; Chen, Wei-Wei ; Han, Ying ; Zhou, Ye-Bo ; Zhang, Feng ; Gao, Xing-Ya ; Zhu, Guo-Qing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5132-d7c4aa3aae7445547b72ed0384d73bafe31017d3804f312c99eabb2a42d292333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adipose Tissue, White - drug effects</topic><topic>Adipose Tissue, White - innervation</topic><topic>Adipose Tissue, White - physiopathology</topic><topic>Angiotensin II - blood</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Pressure - physiology</topic><topic>Capsaicin - pharmacology</topic><topic>Cardiology. Vascular system</topic><topic>Diet, High-Fat - adverse effects</topic><topic>Diterpenes - pharmacology</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Hypertension - blood</topic><topic>Hypertension - etiology</topic><topic>Hypertension - physiopathology</topic><topic>Immunohistochemistry</topic><topic>Lidocaine - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Norepinephrine - blood</topic><topic>Obesity</topic><topic>Obesity - etiology</topic><topic>Obesity - physiopathology</topic><topic>Paraventricular Hypothalamic Nucleus - drug effects</topic><topic>Paraventricular Hypothalamic Nucleus - metabolism</topic><topic>Proto-Oncogene Proteins c-fos - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reflex - physiology</topic><topic>Renin - blood</topic><topic>Sensory System Agents - pharmacology</topic><topic>Sympathetic Nervous System - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xiong, Xiao-Qing</creatorcontrib><creatorcontrib>Chen, Wei-Wei</creatorcontrib><creatorcontrib>Han, Ying</creatorcontrib><creatorcontrib>Zhou, Ye-Bo</creatorcontrib><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Gao, Xing-Ya</creatorcontrib><creatorcontrib>Zhu, Guo-Qing</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xiong, Xiao-Qing</au><au>Chen, Wei-Wei</au><au>Han, Ying</au><au>Zhou, Ye-Bo</au><au>Zhang, Feng</au><au>Gao, Xing-Ya</au><au>Zhu, Guo-Qing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhanced Adipose Afferent Reflex Contributes to Sympathetic Activation in Diet-Induced Obesity Hypertension</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2012-11</date><risdate>2012</risdate><volume>60</volume><issue>5</issue><spage>1280</spage><epage>1286</epage><pages>1280-1286</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>We recently found that adipose afferent reflex (AAR) induced by chemical stimulation of white adipose tissue (WAT) increased sympathetic outflow and blood pressure in normal rats. The study was designed to test the hypothesis that AAR contributes to sympathetic activation in obesity hypertension. Male rats were fed with a control diet (12% kcal as fat) or high-fat diet (42% kcal as fat) for 12 weeks to induce obesity hypertension. Stimulation of WAT with capsaicin increased renal sympathetic nerve activity and mean arterial pressure. Both AAR and WAT afferent activity were enhanced in obesity hypertension (OH) compared with obesity nonhypertension (ON) and in ON compared with obesity-resistant or control diet rats. WAT sensory denervation induced by resiniferatoxin caused greater decreases in renal sympathetic nerve activity and mean arterial pressure in OH than ON and in ON than obesity-resistant or control. The depressor effect of resiniferatoxin lasted ≥3 weeks in OH. Leptin antagonist in WAT reduced renal sympathetic nerve activity and mean arterial pressure in OH. WAT injection of capsaicin increased plasma renin, angiotensin II, and norepinephrine levels in OH and caused more c-fos expression in paraventricular nucleus in OH than ON and in ON than obesity-resistant or control rats. Inhibiting paraventricular nucleus neurons with lidocaine attenuated renal sympathetic nerve activity in OH and ON, decreased mean arterial pressure in OH, and abolished the capsaicin-induced AAR in all groups. The results indicate that enhanced AAR contributes to sympathetic activation in OH, and paraventricular nucleus plays an important role in the enhanced AAR and sympathetic activation in OH.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>23033372</pmid><doi>10.1161/HYPERTENSIONAHA.112.198002</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0194-911X |
| ispartof | Hypertension (Dallas, Tex. 1979), 2012-11, Vol.60 (5), p.1280-1286 |
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| subjects | Adipose Tissue, White - drug effects Adipose Tissue, White - innervation Adipose Tissue, White - physiopathology Angiotensin II - blood Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure - drug effects Blood Pressure - physiology Capsaicin - pharmacology Cardiology. Vascular system Diet, High-Fat - adverse effects Diterpenes - pharmacology Enzyme-Linked Immunosorbent Assay Hypertension - blood Hypertension - etiology Hypertension - physiopathology Immunohistochemistry Lidocaine - pharmacology Male Medical sciences Metabolic diseases Norepinephrine - blood Obesity Obesity - etiology Obesity - physiopathology Paraventricular Hypothalamic Nucleus - drug effects Paraventricular Hypothalamic Nucleus - metabolism Proto-Oncogene Proteins c-fos - metabolism Rats Rats, Sprague-Dawley Reflex - physiology Renin - blood Sensory System Agents - pharmacology Sympathetic Nervous System - physiopathology |
| title | Enhanced Adipose Afferent Reflex Contributes to Sympathetic Activation in Diet-Induced Obesity Hypertension |
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