Neostigmine and pilocarpine attenuated tumour necrosis factor α expression and cardiac hypertrophy in the heart with pressure overload
The inflammatory cytokine tumour necrosis factor α (TNFα) is known to be a major factor contributing to cardiac remodelling and dysfunction. Parasympathetic nervous system cholinergic function can inhibit TNFα expression during systemic infection. In the present study, we tested the effects of a cho...
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Veröffentlicht in: | Experimental physiology 2008-01, Vol.93 (1), p.75-82 |
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description | The inflammatory cytokine tumour necrosis factor α (TNFα) is known to be a major factor contributing to cardiac remodelling and dysfunction. Parasympathetic nervous system cholinergic function can inhibit TNFα expression during systemic infection. In the present study, we tested the effects of a cholinesterase inhibitor, neostigmine, and a muscarinic cholinergic agonist, pilocarpine, on cardiac hypertrophy and TNFα levels during pressure overload. Rats with transverse aortic constriction exhibited elevated TNFα protein levels in the heart, increased heart weight to body weight ratios (an index of cardiac hypertrophy) and decreased left ventricular diastolic function. Two weeks of infusion with neostigmine (6 μg kg−1 day−1) or pilocarpine (0.3 mg kg−1 day−1) significantly reduced cardiac hypertrophy, reduced TNFα levels and elevated interleukin‐10 levels in heart tissues, and improved ventricular function in rats with transverse aortic constriction. Neither of these treatments significantly changed ventricular pressure load. Furthermore, in primary cultured neonatal cardiac cells, treatment with pilocarpine attenuated adrenergic agonist phenylephrine‐induced increased TNFα expression and [3H]leucine (a marker of protein synthesis) incorporation in the cells. Collectively, both cholinergic agents decreased TNFα levels and attenuated cardiac hypertrophy. Since both agents potentially enhanced cholinergic function, the anti‐inflammatory action may be involved in the cardioprotective effect of the treatments with these agents. |
doi_str_mv | 10.1113/expphysiol.2007.039784 |
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Parasympathetic nervous system cholinergic function can inhibit TNFα expression during systemic infection. In the present study, we tested the effects of a cholinesterase inhibitor, neostigmine, and a muscarinic cholinergic agonist, pilocarpine, on cardiac hypertrophy and TNFα levels during pressure overload. Rats with transverse aortic constriction exhibited elevated TNFα protein levels in the heart, increased heart weight to body weight ratios (an index of cardiac hypertrophy) and decreased left ventricular diastolic function. Two weeks of infusion with neostigmine (6 μg kg−1 day−1) or pilocarpine (0.3 mg kg−1 day−1) significantly reduced cardiac hypertrophy, reduced TNFα levels and elevated interleukin‐10 levels in heart tissues, and improved ventricular function in rats with transverse aortic constriction. Neither of these treatments significantly changed ventricular pressure load. Furthermore, in primary cultured neonatal cardiac cells, treatment with pilocarpine attenuated adrenergic agonist phenylephrine‐induced increased TNFα expression and [3H]leucine (a marker of protein synthesis) incorporation in the cells. Collectively, both cholinergic agents decreased TNFα levels and attenuated cardiac hypertrophy. Since both agents potentially enhanced cholinergic function, the anti‐inflammatory action may be involved in the cardioprotective effect of the treatments with these agents.</description><identifier>ISSN: 0958-0670</identifier><identifier>EISSN: 1469-445X</identifier><identifier>DOI: 10.1113/expphysiol.2007.039784</identifier><identifier>PMID: 17872965</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Animals, Newborn ; Body Weight - physiology ; Cardiomegaly - prevention & control ; Cells, Cultured ; Constriction, Pathologic - physiopathology ; Drug Interactions ; Enzyme-Linked Immunosorbent Assay ; Heart - drug effects ; Heart - physiology ; Interleukin-10 - biosynthesis ; Male ; Neostigmine - pharmacology ; Organ Size - physiology ; Parasympathomimetics - pharmacology ; Phenylephrine - pharmacology ; Pilocarpine - pharmacology ; Pressure ; Rats ; Rats, Sprague-Dawley ; Sympathomimetics - pharmacology ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor Necrosis Factor-alpha - biosynthesis ; Ventricular Function</subject><ispartof>Experimental physiology, 2008-01, Vol.93 (1), p.75-82</ispartof><rights>2007 The Authors. 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Parasympathetic nervous system cholinergic function can inhibit TNFα expression during systemic infection. In the present study, we tested the effects of a cholinesterase inhibitor, neostigmine, and a muscarinic cholinergic agonist, pilocarpine, on cardiac hypertrophy and TNFα levels during pressure overload. Rats with transverse aortic constriction exhibited elevated TNFα protein levels in the heart, increased heart weight to body weight ratios (an index of cardiac hypertrophy) and decreased left ventricular diastolic function. Two weeks of infusion with neostigmine (6 μg kg−1 day−1) or pilocarpine (0.3 mg kg−1 day−1) significantly reduced cardiac hypertrophy, reduced TNFα levels and elevated interleukin‐10 levels in heart tissues, and improved ventricular function in rats with transverse aortic constriction. Neither of these treatments significantly changed ventricular pressure load. Furthermore, in primary cultured neonatal cardiac cells, treatment with pilocarpine attenuated adrenergic agonist phenylephrine‐induced increased TNFα expression and [3H]leucine (a marker of protein synthesis) incorporation in the cells. Collectively, both cholinergic agents decreased TNFα levels and attenuated cardiac hypertrophy. Since both agents potentially enhanced cholinergic function, the anti‐inflammatory action may be involved in the cardioprotective effect of the treatments with these agents.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Body Weight - physiology</subject><subject>Cardiomegaly - prevention & control</subject><subject>Cells, Cultured</subject><subject>Constriction, Pathologic - physiopathology</subject><subject>Drug Interactions</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Heart - drug effects</subject><subject>Heart - physiology</subject><subject>Interleukin-10 - biosynthesis</subject><subject>Male</subject><subject>Neostigmine - pharmacology</subject><subject>Organ Size - physiology</subject><subject>Parasympathomimetics - pharmacology</subject><subject>Phenylephrine - pharmacology</subject><subject>Pilocarpine - pharmacology</subject><subject>Pressure</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Sympathomimetics - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Ventricular Function</subject><issn>0958-0670</issn><issn>1469-445X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkEtOwzAQhi0EoqVwhcoXSLEd58UOVYUiVcACJHaR44yJURpHtkPJCTgPF-FMpA-pW1ajkeb79c-H0JSSGaU0vIavtq16p009Y4QkMxJmScpP0JjyOAs4j95O0ZhkURqQOCEjdOHcByE0JCk_RyOapAnL4miMvh_BOK_f17oBLJoSt7o2Uth2t3sPTSc8lNh3a9NZ3IC0xmmHlZDeWPz7g4cmFtzQpNnxA1tqIXHVt2C9NUNLrBvsK8AVCOvxRvsK75DOAjafYGsjykt0pkTt4OowJ-j1bvEyXwarp_uH-e0qkHyoHrCkiCUoVWQxpHHKIs6pKmKAImJcpFFSUJYoBbKQKRt-pCGTGS-VYpJEpVDhBMX73O0fzoLKW6vXwvY5JfnWbH40m2_N5nuzAzjdg21XrKE8YgeVw8HN_mCja-j_GZsvnpc85OEfDouQ7Q</recordid><startdate>200801</startdate><enddate>200801</enddate><creator>Freeling, Jessica</creator><creator>Wattier, Kristina</creator><creator>LaCroix, Carly</creator><creator>Li, Yi‐Fan</creator><general>Blackwell Publishing Ltd</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></search><sort><creationdate>200801</creationdate><title>Neostigmine and pilocarpine attenuated tumour necrosis factor α expression and cardiac hypertrophy in the heart with pressure overload</title><author>Freeling, Jessica ; Wattier, Kristina ; LaCroix, Carly ; Li, Yi‐Fan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4084-27b6ceffb96e86825441fb6eeb524a857b127ffecbc82872132c94dff2c05daf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Body Weight - physiology</topic><topic>Cardiomegaly - prevention & control</topic><topic>Cells, Cultured</topic><topic>Constriction, Pathologic - physiopathology</topic><topic>Drug Interactions</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Heart - drug effects</topic><topic>Heart - physiology</topic><topic>Interleukin-10 - biosynthesis</topic><topic>Male</topic><topic>Neostigmine - pharmacology</topic><topic>Organ Size - physiology</topic><topic>Parasympathomimetics - pharmacology</topic><topic>Phenylephrine - pharmacology</topic><topic>Pilocarpine - pharmacology</topic><topic>Pressure</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Sympathomimetics - pharmacology</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Ventricular Function</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Freeling, Jessica</creatorcontrib><creatorcontrib>Wattier, Kristina</creatorcontrib><creatorcontrib>LaCroix, Carly</creatorcontrib><creatorcontrib>Li, Yi‐Fan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Experimental physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Freeling, Jessica</au><au>Wattier, Kristina</au><au>LaCroix, Carly</au><au>Li, Yi‐Fan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neostigmine and pilocarpine attenuated tumour necrosis factor α expression and cardiac hypertrophy in the heart with pressure overload</atitle><jtitle>Experimental physiology</jtitle><addtitle>Exp Physiol</addtitle><date>2008-01</date><risdate>2008</risdate><volume>93</volume><issue>1</issue><spage>75</spage><epage>82</epage><pages>75-82</pages><issn>0958-0670</issn><eissn>1469-445X</eissn><abstract>The inflammatory cytokine tumour necrosis factor α (TNFα) is known to be a major factor contributing to cardiac remodelling and dysfunction. Parasympathetic nervous system cholinergic function can inhibit TNFα expression during systemic infection. In the present study, we tested the effects of a cholinesterase inhibitor, neostigmine, and a muscarinic cholinergic agonist, pilocarpine, on cardiac hypertrophy and TNFα levels during pressure overload. Rats with transverse aortic constriction exhibited elevated TNFα protein levels in the heart, increased heart weight to body weight ratios (an index of cardiac hypertrophy) and decreased left ventricular diastolic function. Two weeks of infusion with neostigmine (6 μg kg−1 day−1) or pilocarpine (0.3 mg kg−1 day−1) significantly reduced cardiac hypertrophy, reduced TNFα levels and elevated interleukin‐10 levels in heart tissues, and improved ventricular function in rats with transverse aortic constriction. Neither of these treatments significantly changed ventricular pressure load. Furthermore, in primary cultured neonatal cardiac cells, treatment with pilocarpine attenuated adrenergic agonist phenylephrine‐induced increased TNFα expression and [3H]leucine (a marker of protein synthesis) incorporation in the cells. Collectively, both cholinergic agents decreased TNFα levels and attenuated cardiac hypertrophy. Since both agents potentially enhanced cholinergic function, the anti‐inflammatory action may be involved in the cardioprotective effect of the treatments with these agents.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>17872965</pmid><doi>10.1113/expphysiol.2007.039784</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Animals, Newborn Body Weight - physiology Cardiomegaly - prevention & control Cells, Cultured Constriction, Pathologic - physiopathology Drug Interactions Enzyme-Linked Immunosorbent Assay Heart - drug effects Heart - physiology Interleukin-10 - biosynthesis Male Neostigmine - pharmacology Organ Size - physiology Parasympathomimetics - pharmacology Phenylephrine - pharmacology Pilocarpine - pharmacology Pressure Rats Rats, Sprague-Dawley Sympathomimetics - pharmacology Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - biosynthesis Ventricular Function |
title | Neostigmine and pilocarpine attenuated tumour necrosis factor α expression and cardiac hypertrophy in the heart with pressure overload |
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