Effect of barodenervation on cardiovascular responses elicited from the hypothalamic arcuate nucleus of the rat
We have previously reported that chemical stimulation of the hypothalamic arcuate nucleus (ARCN) in the rat elicited increases as well as decreases in blood pressure (BP) and sympathetic nerve activity (SNA). The type of response elicited from the ARCN (i.e., increase or decrease in BP and SNA) depe...
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| description | We have previously reported that chemical stimulation of the hypothalamic arcuate nucleus (ARCN) in the rat elicited increases as well as decreases in blood pressure (BP) and sympathetic nerve activity (SNA). The type of response elicited from the ARCN (i.e., increase or decrease in BP and SNA) depended on the level of baroreceptor activity which, in turn, was determined by baseline BP in rats with intact baroreceptors. Based on this information, it was hypothesized that baroreceptor unloading may play a role in the type of response elicited from the ARCN. Therefore, the effect of barodenervation on the ARCN-induced cardiovascular and sympathetic responses and the neurotransmitters in the hypothalamic paraventricular nucleus (PVN) mediating the excitatory responses elicited from the ARCN were investigated in urethane-anesthetized adult male Wistar rats. Bilateral barodenervation converted decreases in mean arterial pressure (MAP) and greater splanchnic nerve activity (GSNA) elicited by chemical stimulation of the ARCN with microinjections of N-methyl-D-aspartic acid to increases in MAP and GSNA and exaggerated the increases in heart rate (HR). Combined microinjections of NBQX and D-AP7 (ionotropic glutamate receptor antagonists) into the PVN in barodenervated rats converted increases in MAP and GSNA elicited by the ARCN stimulation to decreases in MAP and GSNA and attenuated increases in HR. Microinjections of SHU9119 (a melanocortin 3/4 receptor antagonist) into the PVN in barodenervated rats attenuated increases in MAP, GSNA and HR elicited by the ARCN stimulation. ARCN neurons projecting to the PVN were immunoreactive for proopiomelanocortin, alpha-melanocyte stimulating hormone (alpha-MSH) and adrenocorticotropic hormone (ACTH). It was concluded that increases in MAP and GSNA and exaggeration of tachycardia elicited by the ARCN stimulation in barodenervated rats may be mediated via release of alpha-MSH and/or ACTH and glutamate from the ARCN neurons projecting to the PVN. |
| doi_str_mv | 10.1371/journal.pone.0053111 |
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The type of response elicited from the ARCN (i.e., increase or decrease in BP and SNA) depended on the level of baroreceptor activity which, in turn, was determined by baseline BP in rats with intact baroreceptors. Based on this information, it was hypothesized that baroreceptor unloading may play a role in the type of response elicited from the ARCN. Therefore, the effect of barodenervation on the ARCN-induced cardiovascular and sympathetic responses and the neurotransmitters in the hypothalamic paraventricular nucleus (PVN) mediating the excitatory responses elicited from the ARCN were investigated in urethane-anesthetized adult male Wistar rats. Bilateral barodenervation converted decreases in mean arterial pressure (MAP) and greater splanchnic nerve activity (GSNA) elicited by chemical stimulation of the ARCN with microinjections of N-methyl-D-aspartic acid to increases in MAP and GSNA and exaggerated the increases in heart rate (HR). Combined microinjections of NBQX and D-AP7 (ionotropic glutamate receptor antagonists) into the PVN in barodenervated rats converted increases in MAP and GSNA elicited by the ARCN stimulation to decreases in MAP and GSNA and attenuated increases in HR. Microinjections of SHU9119 (a melanocortin 3/4 receptor antagonist) into the PVN in barodenervated rats attenuated increases in MAP, GSNA and HR elicited by the ARCN stimulation. ARCN neurons projecting to the PVN were immunoreactive for proopiomelanocortin, alpha-melanocyte stimulating hormone (alpha-MSH) and adrenocorticotropic hormone (ACTH). It was concluded that increases in MAP and GSNA and exaggeration of tachycardia elicited by the ARCN stimulation in barodenervated rats may be mediated via release of alpha-MSH and/or ACTH and glutamate from the ARCN neurons projecting to the PVN.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0053111</identifier><identifier>PMID: 23300873</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>2-Amino-5-phosphonovalerate - analogs & derivatives ; 2-Amino-5-phosphonovalerate - pharmacology ; Adrenocorticotropic hormone ; Adrenocorticotropic Hormone - metabolism ; alpha-MSH ; Animals ; Arcuate nucleus ; Arcuate Nucleus of Hypothalamus - drug effects ; Arcuate Nucleus of Hypothalamus - metabolism ; Arcuate Nucleus of Hypothalamus - physiopathology ; Aspartate ; Aspartic acid ; Baroreceptors ; Biology ; Blood pressure ; Blood Pressure - drug effects ; Blood Pressure - physiology ; Brain ; Cardiovascular system ; Cardiovascular System - drug effects ; Cardiovascular System - innervation ; Cocaine ; Corticotropin ; D-aspartic acid ; Denervation ; Dentistry ; Drug dosages ; Ethyl carbamate ; Excitatory Amino Acid Antagonists - pharmacology ; Glutamate ; Glutamic acid receptors ; Heart rate ; Heart Rate - drug effects ; Heart Rate - physiology ; Hypertension ; Hypothalamus ; Laboratory animals ; Male ; Medical research ; Medical schools ; Medicine ; Melanocortin ; Melanocyte stimulating hormone ; Melanocyte-Stimulating Hormones - pharmacology ; N-methyl-D-aspartate ; N-Methyl-D-aspartic acid ; Narcotics ; Neurons ; Neuropeptides ; Neurotransmitters ; Nuclei ; Paraventricular Hypothalamic Nucleus - metabolism ; Paraventricular nucleus ; Pressoreceptors - physiopathology ; Pro-Opiomelanocortin - metabolism ; Proopiomelanocortin ; Quinoxalines - pharmacology ; Rats ; Rats, Wistar ; Receptors, Corticotropin - antagonists & inhibitors ; Rodents ; Splanchnic nerve ; Splanchnic Nerves - drug effects ; Splanchnic Nerves - physiopathology ; Stimulation ; Surgery ; Sympathetic Nervous System - drug effects ; Sympathetic Nervous System - metabolism ; Sympathetic Nervous System - physiopathology ; Tachycardia ; Unloading ; Ventilators</subject><ispartof>PloS one, 2012-12, Vol.7 (12), p.e53111-e53111</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Kawabe et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2012 Kawabe et al 2012 Kawabe et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-b8c99724f7867d2883443b6cb879785b12a01e81bb9d37dd82bfbbabfddbe9943</citedby><cites>FETCH-LOGICAL-c758t-b8c99724f7867d2883443b6cb879785b12a01e81bb9d37dd82bfbbabfddbe9943</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3531379/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3531379/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23300873$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Chowen, Julie A.</contributor><creatorcontrib>Kawabe, Tetsuya</creatorcontrib><creatorcontrib>Kawabe, Kazumi</creatorcontrib><creatorcontrib>Sapru, Hreday N</creatorcontrib><title>Effect of barodenervation on cardiovascular responses elicited from the hypothalamic arcuate nucleus of the rat</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>We have previously reported that chemical stimulation of the hypothalamic arcuate nucleus (ARCN) in the rat elicited increases as well as decreases in blood pressure (BP) and sympathetic nerve activity (SNA). The type of response elicited from the ARCN (i.e., increase or decrease in BP and SNA) depended on the level of baroreceptor activity which, in turn, was determined by baseline BP in rats with intact baroreceptors. Based on this information, it was hypothesized that baroreceptor unloading may play a role in the type of response elicited from the ARCN. Therefore, the effect of barodenervation on the ARCN-induced cardiovascular and sympathetic responses and the neurotransmitters in the hypothalamic paraventricular nucleus (PVN) mediating the excitatory responses elicited from the ARCN were investigated in urethane-anesthetized adult male Wistar rats. Bilateral barodenervation converted decreases in mean arterial pressure (MAP) and greater splanchnic nerve activity (GSNA) elicited by chemical stimulation of the ARCN with microinjections of N-methyl-D-aspartic acid to increases in MAP and GSNA and exaggerated the increases in heart rate (HR). Combined microinjections of NBQX and D-AP7 (ionotropic glutamate receptor antagonists) into the PVN in barodenervated rats converted increases in MAP and GSNA elicited by the ARCN stimulation to decreases in MAP and GSNA and attenuated increases in HR. Microinjections of SHU9119 (a melanocortin 3/4 receptor antagonist) into the PVN in barodenervated rats attenuated increases in MAP, GSNA and HR elicited by the ARCN stimulation. ARCN neurons projecting to the PVN were immunoreactive for proopiomelanocortin, alpha-melanocyte stimulating hormone (alpha-MSH) and adrenocorticotropic hormone (ACTH). It was concluded that increases in MAP and GSNA and exaggeration of tachycardia elicited by the ARCN stimulation in barodenervated rats may be mediated via release of alpha-MSH and/or ACTH and glutamate from the ARCN neurons projecting to the PVN.</description><subject>2-Amino-5-phosphonovalerate - analogs & derivatives</subject><subject>2-Amino-5-phosphonovalerate - pharmacology</subject><subject>Adrenocorticotropic hormone</subject><subject>Adrenocorticotropic Hormone - metabolism</subject><subject>alpha-MSH</subject><subject>Animals</subject><subject>Arcuate nucleus</subject><subject>Arcuate Nucleus of Hypothalamus - drug effects</subject><subject>Arcuate Nucleus of Hypothalamus - metabolism</subject><subject>Arcuate Nucleus of Hypothalamus - physiopathology</subject><subject>Aspartate</subject><subject>Aspartic acid</subject><subject>Baroreceptors</subject><subject>Biology</subject><subject>Blood pressure</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Brain</subject><subject>Cardiovascular system</subject><subject>Cardiovascular System - drug effects</subject><subject>Cardiovascular System - innervation</subject><subject>Cocaine</subject><subject>Corticotropin</subject><subject>D-aspartic acid</subject><subject>Denervation</subject><subject>Dentistry</subject><subject>Drug dosages</subject><subject>Ethyl carbamate</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Glutamate</subject><subject>Glutamic acid receptors</subject><subject>Heart rate</subject><subject>Heart Rate - drug effects</subject><subject>Heart Rate - physiology</subject><subject>Hypertension</subject><subject>Hypothalamus</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Medical research</subject><subject>Medical schools</subject><subject>Medicine</subject><subject>Melanocortin</subject><subject>Melanocyte stimulating hormone</subject><subject>Melanocyte-Stimulating Hormones - pharmacology</subject><subject>N-methyl-D-aspartate</subject><subject>N-Methyl-D-aspartic acid</subject><subject>Narcotics</subject><subject>Neurons</subject><subject>Neuropeptides</subject><subject>Neurotransmitters</subject><subject>Nuclei</subject><subject>Paraventricular Hypothalamic Nucleus - metabolism</subject><subject>Paraventricular nucleus</subject><subject>Pressoreceptors - physiopathology</subject><subject>Pro-Opiomelanocortin - metabolism</subject><subject>Proopiomelanocortin</subject><subject>Quinoxalines - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Corticotropin - antagonists & inhibitors</subject><subject>Rodents</subject><subject>Splanchnic nerve</subject><subject>Splanchnic Nerves - drug effects</subject><subject>Splanchnic Nerves - physiopathology</subject><subject>Stimulation</subject><subject>Surgery</subject><subject>Sympathetic Nervous System - drug effects</subject><subject>Sympathetic Nervous System - metabolism</subject><subject>Sympathetic Nervous System - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agriculture Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Access via ProQuest (Open Access)</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kawabe, Tetsuya</au><au>Kawabe, Kazumi</au><au>Sapru, Hreday N</au><au>Chowen, Julie A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of barodenervation on cardiovascular responses elicited from the hypothalamic arcuate nucleus of the rat</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-12-27</date><risdate>2012</risdate><volume>7</volume><issue>12</issue><spage>e53111</spage><epage>e53111</epage><pages>e53111-e53111</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>We have previously reported that chemical stimulation of the hypothalamic arcuate nucleus (ARCN) in the rat elicited increases as well as decreases in blood pressure (BP) and sympathetic nerve activity (SNA). The type of response elicited from the ARCN (i.e., increase or decrease in BP and SNA) depended on the level of baroreceptor activity which, in turn, was determined by baseline BP in rats with intact baroreceptors. Based on this information, it was hypothesized that baroreceptor unloading may play a role in the type of response elicited from the ARCN. Therefore, the effect of barodenervation on the ARCN-induced cardiovascular and sympathetic responses and the neurotransmitters in the hypothalamic paraventricular nucleus (PVN) mediating the excitatory responses elicited from the ARCN were investigated in urethane-anesthetized adult male Wistar rats. Bilateral barodenervation converted decreases in mean arterial pressure (MAP) and greater splanchnic nerve activity (GSNA) elicited by chemical stimulation of the ARCN with microinjections of N-methyl-D-aspartic acid to increases in MAP and GSNA and exaggerated the increases in heart rate (HR). Combined microinjections of NBQX and D-AP7 (ionotropic glutamate receptor antagonists) into the PVN in barodenervated rats converted increases in MAP and GSNA elicited by the ARCN stimulation to decreases in MAP and GSNA and attenuated increases in HR. Microinjections of SHU9119 (a melanocortin 3/4 receptor antagonist) into the PVN in barodenervated rats attenuated increases in MAP, GSNA and HR elicited by the ARCN stimulation. ARCN neurons projecting to the PVN were immunoreactive for proopiomelanocortin, alpha-melanocyte stimulating hormone (alpha-MSH) and adrenocorticotropic hormone (ACTH). It was concluded that increases in MAP and GSNA and exaggeration of tachycardia elicited by the ARCN stimulation in barodenervated rats may be mediated via release of alpha-MSH and/or ACTH and glutamate from the ARCN neurons projecting to the PVN.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23300873</pmid><doi>10.1371/journal.pone.0053111</doi><tpages>e53111</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2012-12, Vol.7 (12), p.e53111-e53111 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1327231110 |
| source | PubMed Central Free; MEDLINE; Public Library of Science; DOAJ Directory of Open Access Journals; Free Full-Text Journals in Chemistry; EZB Electronic Journals Library |
| subjects | 2-Amino-5-phosphonovalerate - analogs & derivatives 2-Amino-5-phosphonovalerate - pharmacology Adrenocorticotropic hormone Adrenocorticotropic Hormone - metabolism alpha-MSH Animals Arcuate nucleus Arcuate Nucleus of Hypothalamus - drug effects Arcuate Nucleus of Hypothalamus - metabolism Arcuate Nucleus of Hypothalamus - physiopathology Aspartate Aspartic acid Baroreceptors Biology Blood pressure Blood Pressure - drug effects Blood Pressure - physiology Brain Cardiovascular system Cardiovascular System - drug effects Cardiovascular System - innervation Cocaine Corticotropin D-aspartic acid Denervation Dentistry Drug dosages Ethyl carbamate Excitatory Amino Acid Antagonists - pharmacology Glutamate Glutamic acid receptors Heart rate Heart Rate - drug effects Heart Rate - physiology Hypertension Hypothalamus Laboratory animals Male Medical research Medical schools Medicine Melanocortin Melanocyte stimulating hormone Melanocyte-Stimulating Hormones - pharmacology N-methyl-D-aspartate N-Methyl-D-aspartic acid Narcotics Neurons Neuropeptides Neurotransmitters Nuclei Paraventricular Hypothalamic Nucleus - metabolism Paraventricular nucleus Pressoreceptors - physiopathology Pro-Opiomelanocortin - metabolism Proopiomelanocortin Quinoxalines - pharmacology Rats Rats, Wistar Receptors, Corticotropin - antagonists & inhibitors Rodents Splanchnic nerve Splanchnic Nerves - drug effects Splanchnic Nerves - physiopathology Stimulation Surgery Sympathetic Nervous System - drug effects Sympathetic Nervous System - metabolism Sympathetic Nervous System - physiopathology Tachycardia Unloading Ventilators |
| title | Effect of barodenervation on cardiovascular responses elicited from the hypothalamic arcuate nucleus of the rat |
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