Angiotensin-Converting Enzyme Inhibitor Up-Regulates Cardiac β-Receptors in Cultured Neonatal Rat Myocytes
In patients with congestive heart failure (CHF), β-receptor up-regulation is regarded as one of the mechanisms leading to improved function and prognosis. To clarify whether β-receptor up-regulation is involved in the mechanisms underlying the beneficial effects of angiotensin-converting enzyme (ACE...
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Veröffentlicht in: | JAPANESE CIRCULATION JOURNAL 1997, Vol.61(2), pp.170-179 |
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description | In patients with congestive heart failure (CHF), β-receptor up-regulation is regarded as one of the mechanisms leading to improved function and prognosis. To clarify whether β-receptor up-regulation is involved in the mechanisms underlying the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors, we investigated the actions of ACE inhibitors and an angiotensin II type I receptor (AT1) antagonist on β-receptors of neonatal rat cultured cardiac myocytes. Angiotensin II (A-II) increased the spontaneous beating frequency of the cells, and the effect was completely antagonized by the AT1 antagonist CV-11974. Under control conditions, β-receptor density (Bmax) and affinity (Kd) were measured by radiobinding assay with the hydrophilic ligand [3H]CGP-12177, and were 103 ±11 fmol/mg protein and 3.4±0.4 nmol/L, respectively. Captopril increased the β-receptor density of myocytes and augmented the response to isoproterenol. Bmax was increased by 34% after 24 h treatment with 10 -6 mol/L captopril. CV-3480, an ACE inhibitor that contains no sulthydryl group, but neither A-II nor the AT1 antagonist, also up-regulated β-receptors. The results suggest that β-receptor up-regulation contributes at least partly to the beneficial cardiac effects of ACE inhibitors in patients with CHF. ACE inhibitors and AT1 antagonists seem to play different roles in clinical practice. (Jpn Circ J 1997; 61: 170 -179) |
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To clarify whether β-receptor up-regulation is involved in the mechanisms underlying the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors, we investigated the actions of ACE inhibitors and an angiotensin II type I receptor (AT1) antagonist on β-receptors of neonatal rat cultured cardiac myocytes. Angiotensin II (A-II) increased the spontaneous beating frequency of the cells, and the effect was completely antagonized by the AT1 antagonist CV-11974. Under control conditions, β-receptor density (Bmax) and affinity (Kd) were measured by radiobinding assay with the hydrophilic ligand [3H]CGP-12177, and were 103 ±11 fmol/mg protein and 3.4±0.4 nmol/L, respectively. Captopril increased the β-receptor density of myocytes and augmented the response to isoproterenol. Bmax was increased by 34% after 24 h treatment with 10 -6 mol/L captopril. CV-3480, an ACE inhibitor that contains no sulthydryl group, but neither A-II nor the AT1 antagonist, also up-regulated β-receptors. The results suggest that β-receptor up-regulation contributes at least partly to the beneficial cardiac effects of ACE inhibitors in patients with CHF. ACE inhibitors and AT1 antagonists seem to play different roles in clinical practice. 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Drug treatments ; Radioligand Assay ; Rats ; Receptors, Adrenergic, beta - metabolism ; Tetrazoles - pharmacology ; Up-Regulation ; Vasodilator agents. 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To clarify whether β-receptor up-regulation is involved in the mechanisms underlying the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors, we investigated the actions of ACE inhibitors and an angiotensin II type I receptor (AT1) antagonist on β-receptors of neonatal rat cultured cardiac myocytes. Angiotensin II (A-II) increased the spontaneous beating frequency of the cells, and the effect was completely antagonized by the AT1 antagonist CV-11974. Under control conditions, β-receptor density (Bmax) and affinity (Kd) were measured by radiobinding assay with the hydrophilic ligand [3H]CGP-12177, and were 103 ±11 fmol/mg protein and 3.4±0.4 nmol/L, respectively. Captopril increased the β-receptor density of myocytes and augmented the response to isoproterenol. Bmax was increased by 34% after 24 h treatment with 10 -6 mol/L captopril. CV-3480, an ACE inhibitor that contains no sulthydryl group, but neither A-II nor the AT1 antagonist, also up-regulated β-receptors. The results suggest that β-receptor up-regulation contributes at least partly to the beneficial cardiac effects of ACE inhibitors in patients with CHF. ACE inhibitors and AT1 antagonists seem to play different roles in clinical practice. (Jpn Circ J 1997; 61: 170 -179)</description><subject>Angiotensin II</subject><subject>Angiotensin II - pharmacology</subject><subject>Angiotensin II receptor antagonist</subject><subject>Angiotensin Receptor Antagonists</subject><subject>Angiotensin-Converting Enzyme Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>b-Adrenergic receptor</subject><subject>Benzimidazoles - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Captopril - pharmacology</subject><subject>Cardiovascular system</subject><subject>Cells, Cultured</subject><subject>Congestive heart failure</subject><subject>Medical sciences</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardium - cytology</subject><subject>Myocardium - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Radioligand Assay</subject><subject>Rats</subject><subject>Receptors, Adrenergic, beta - metabolism</subject><subject>Tetrazoles - pharmacology</subject><subject>Up-Regulation</subject><subject>Vasodilator agents. Cerebral vasodilators</subject><issn>0047-1828</issn><issn>1347-4839</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kM1uEzEURi0EKqGwYY_kBeoCaYL_xp5ZoWpU2koFpIqurRvPndRh4gm2Byk8Fg_CM-EqIRvb8nd8P-sQ8pazJRe1_Lhxm6XmS27YM7LgUplKNbJ9ThaMlTNvRPOSvEppw5gwqq7PyFnLDGuNXJAfl2Htp4wh-VB1U_iFMfuwplfh936L9DY8-pXPU6QPu-oe1_MIGRPtIPYeHP37p1w63BUgUR9oN495jtjTrzgFyDDSe8j0y35y-_LsNXkxwJjwzXE_Jw-fr753N9Xdt-vb7vKuckq3uTJNA9pps-IGWsm1Etq0gomm1di3jgMoVAPgUCvONTbYrpqhdgZl-UqvuTwnF4e5uzj9nDFlu_XJ4ThCwGlOthQY2ci6gB8OoItTShEHu4t-C3FvObNPZm0xazW3xWyB3x2nzqst9if0qLLk7485JAfjECE4n06Y0EoL9tT56YBtUoY1nnIo3t2I_xvFYSnFp8Q9QrQY5D-F35mR</recordid><startdate>1997</startdate><enddate>1997</enddate><creator>Yonemochi, Hidetoshi</creator><creator>Saikawa, Tetsunori</creator><creator>Yasunaga, Seikou</creator><creator>Iwao, Tetsu</creator><creator>Takakura, Takeshi</creator><creator>Nakagawa, Mikiko</creator><creator>Sakata, Toshiie</creator><creator>Ito, Morio</creator><general>The Japanese Circulation Society</general><general>Japanese Circulation Society</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>1997</creationdate><title>Angiotensin-Converting Enzyme Inhibitor Up-Regulates Cardiac β-Receptors in Cultured Neonatal Rat Myocytes</title><author>Yonemochi, Hidetoshi ; Saikawa, Tetsunori ; Yasunaga, Seikou ; Iwao, Tetsu ; Takakura, Takeshi ; Nakagawa, Mikiko ; Sakata, Toshiie ; Ito, Morio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c469t-788a6c67b17a931642679202896ed9c1aa4e4faef54116e8e9b8f5c7e3eced613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Angiotensin II</topic><topic>Angiotensin II - pharmacology</topic><topic>Angiotensin II receptor antagonist</topic><topic>Angiotensin Receptor Antagonists</topic><topic>Angiotensin-Converting Enzyme Inhibitors - pharmacology</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>b-Adrenergic receptor</topic><topic>Benzimidazoles - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Captopril - pharmacology</topic><topic>Cardiovascular system</topic><topic>Cells, Cultured</topic><topic>Congestive heart failure</topic><topic>Medical sciences</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardium - cytology</topic><topic>Myocardium - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Radioligand Assay</topic><topic>Rats</topic><topic>Receptors, Adrenergic, beta - metabolism</topic><topic>Tetrazoles - pharmacology</topic><topic>Up-Regulation</topic><topic>Vasodilator agents. Cerebral vasodilators</topic><toplevel>online_resources</toplevel><creatorcontrib>Yonemochi, Hidetoshi</creatorcontrib><creatorcontrib>Saikawa, Tetsunori</creatorcontrib><creatorcontrib>Yasunaga, Seikou</creatorcontrib><creatorcontrib>Iwao, Tetsu</creatorcontrib><creatorcontrib>Takakura, Takeshi</creatorcontrib><creatorcontrib>Nakagawa, Mikiko</creatorcontrib><creatorcontrib>Sakata, Toshiie</creatorcontrib><creatorcontrib>Ito, Morio</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>JAPANESE CIRCULATION JOURNAL</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yonemochi, Hidetoshi</au><au>Saikawa, Tetsunori</au><au>Yasunaga, Seikou</au><au>Iwao, Tetsu</au><au>Takakura, Takeshi</au><au>Nakagawa, Mikiko</au><au>Sakata, Toshiie</au><au>Ito, Morio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin-Converting Enzyme Inhibitor Up-Regulates Cardiac β-Receptors in Cultured Neonatal Rat Myocytes</atitle><jtitle>JAPANESE CIRCULATION JOURNAL</jtitle><addtitle>JAPANESE CIRCULATION JOURNAL</addtitle><date>1997</date><risdate>1997</risdate><volume>61</volume><issue>2</issue><spage>170</spage><epage>179</epage><pages>170-179</pages><issn>0047-1828</issn><eissn>1347-4839</eissn><coden>JCIRA2</coden><abstract>In patients with congestive heart failure (CHF), β-receptor up-regulation is regarded as one of the mechanisms leading to improved function and prognosis. To clarify whether β-receptor up-regulation is involved in the mechanisms underlying the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors, we investigated the actions of ACE inhibitors and an angiotensin II type I receptor (AT1) antagonist on β-receptors of neonatal rat cultured cardiac myocytes. Angiotensin II (A-II) increased the spontaneous beating frequency of the cells, and the effect was completely antagonized by the AT1 antagonist CV-11974. Under control conditions, β-receptor density (Bmax) and affinity (Kd) were measured by radiobinding assay with the hydrophilic ligand [3H]CGP-12177, and were 103 ±11 fmol/mg protein and 3.4±0.4 nmol/L, respectively. Captopril increased the β-receptor density of myocytes and augmented the response to isoproterenol. Bmax was increased by 34% after 24 h treatment with 10 -6 mol/L captopril. CV-3480, an ACE inhibitor that contains no sulthydryl group, but neither A-II nor the AT1 antagonist, also up-regulated β-receptors. The results suggest that β-receptor up-regulation contributes at least partly to the beneficial cardiac effects of ACE inhibitors in patients with CHF. ACE inhibitors and AT1 antagonists seem to play different roles in clinical practice. (Jpn Circ J 1997; 61: 170 -179)</abstract><cop>Kyoto</cop><pub>The Japanese Circulation Society</pub><pmid>9070973</pmid><doi>10.1253/jcj.61.170</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Angiotensin II Angiotensin II - pharmacology Angiotensin II receptor antagonist Angiotensin Receptor Antagonists Angiotensin-Converting Enzyme Inhibitors - pharmacology Animals Animals, Newborn b-Adrenergic receptor Benzimidazoles - pharmacology Biological and medical sciences Captopril - pharmacology Cardiovascular system Cells, Cultured Congestive heart failure Medical sciences Myocardial Contraction - drug effects Myocardium - cytology Myocardium - metabolism Pharmacology. Drug treatments Radioligand Assay Rats Receptors, Adrenergic, beta - metabolism Tetrazoles - pharmacology Up-Regulation Vasodilator agents. Cerebral vasodilators |
title | Angiotensin-Converting Enzyme Inhibitor Up-Regulates Cardiac β-Receptors in Cultured Neonatal Rat Myocytes |
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