{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T03:32:58Z","timestamp":1791343978474,"version":"4.3.1"},"reference-count":18,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2016,3,9]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The regulator of G\u2010protein signaling 5 (Rgs5), which functions as the regulator of G\u2010protein\u2010coupled receptor (\n              <jats:styled-content style=\"fixed-case\">GPCR<\/jats:styled-content>\n              ) including muscarinic receptors, has a potential effect on atrial muscarinic receptor\u2010activated\n              <jats:styled-content style=\"fixed-case\">\n                I\n                <jats:sub>KA<\/jats:sub>\n              <\/jats:styled-content>\n              <jats:sub>ch<\/jats:sub>\n              current.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              In the present study, hearts of Rgs5 knockout (\n              <jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content>\n              ) mice had decreased low\u2010frequency\/high\u2010frequency ratio in spectral measures of heart rate variability. Loss of Rgs5 provoked dramatically exaggerated bradycardia and significantly (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05) prolonged sinus nodal recovery time in response to carbachol (0.1\u00a0mg\/kg, intraperitoneally). Compared to those from wild\u2010type (\n              <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>\n              ) mice, Langendorff perfused hearts from Rgs5\n              <jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content>\n              mice had significantly (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.01) abbreviated atrial effective refractory periods and increased dominant frequency after administration of acetylcholine (\n              <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>\n              h; 1\u00a0\u03bcmol\/L). In addition, whole patch clamp analyses of single atrial myocytes revealed that the\n              <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>\n              h\u2010regulated potassium current (\n              <jats:styled-content style=\"fixed-case\">\n                I\n                <jats:sub>KA<\/jats:sub>\n              <\/jats:styled-content>\n              <jats:sub>ch<\/jats:sub>\n              ) was significant increased in the time course of activation and deactivation (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.01) in Rgs5\n              <jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content>\n              , compared to those in\n              <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>\n              , mice. To further determine the effect of Rgs5, transgenic mice with cardiac\u2010specific overexpression of human Rgs5 were found to be resistant to\n              <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>\n              h\u2010related effects in bradycardia, atrial electrophysiology, and atrial tachyarrhythmia (\n              <jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>\n              ).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The results of this study indicate that, as a critical regulator of parasympathetic activation in the heart, Rgs5 prevents vagal\u2010related bradycardia and\n              <jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>\n              through negatively regulating the\n              <jats:styled-content style=\"fixed-case\">\n                I\n                <jats:sub>KA<\/jats:sub>\n              <\/jats:styled-content>\n              <jats:sub>ch<\/jats:sub>\n              current.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.115.002783","type":"journal-article","created":{"date-parts":[[2018,9,14]],"date-time":"2018-09-14T12:32:07Z","timestamp":1536928327000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":5,"title":["Potential Role of Regulator of G\u2010Protein Signaling 5 in the Protection of Vagal\u2010Related Bradycardia and Atrial Tachyarrhythmia"],"prefix":"10.1161","volume":"5","author":[{"given":"Mu","family":"Qin","sequence":"first","affiliation":[{"name":"Department of Cardiology, Shanghai Chest Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xu","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Shanghai Chest Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tao","family":"Liu","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute of Wuhan University, Wuhan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Teng","family":"Wang","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute of Wuhan University, Wuhan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Congxin","family":"Huang","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute of Wuhan University, Wuhan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.113.302549"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.102.22.2774"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2004.061119"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.105.561738"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1432-1327.2000.01670.x"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.69.1.795"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1515\/CCLM.2009.344"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1008397107"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2012.10.003"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvq271"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0046856"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000207497.50477.60"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.108.180984"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01391.2006"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.110.224212"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(01)01304-3"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvp148"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00779.2009"}],"container-title":["Journal of the American Heart 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