{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T17:43:49Z","timestamp":1793036629757,"version":"4.5.0"},"reference-count":41,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"22","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2018,11,20]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The mechanism underlying the beneficial cardiovascular effects of the incretin GLP\u20101 (glucagon\u2010like peptide 1) and its analogues in humans is elusive. We hypothesized that activating receptors located on vascular smooth muscle cells to induce either peripheral or coronary vasodilatation mediates the cardiovascular effect of\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101.\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              Ten stable patients with angina awaiting left anterior descending artery stenting underwent forearm blood flow measurement using forearm plethysmography and post\u2013percutaneous coronary intervention coronary blood flow measurement using a pressure\u2010flow wire before and after peripheral\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101 administration. Coronary sinus and artery bloods were sampled for\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101 levels. A further 11 control patients received saline rather than\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101 in the coronary blood flow protocol.\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101 receptor (GLP\u20101R) expression was assessed by immunohistochemistry using a specific\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101R monoclonal antibody in human tissue to inform the physiological studies. There was no effect of\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101 on absolute forearm blood flow or forearm blood flow ratio after\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101, systemic hemodynamics were not affected, and no binding of\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101R monoclonal antibody was detected in vascular tissue.\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101 reduced resting coronary transit time (mean [\n              <jats:styled-content style=\"fixed-case\">SD<\/jats:styled-content>\n              ], 0.87 [0.39] versus 0.63\u00a0[0.27] seconds;\n              <jats:italic>P<\/jats:italic>\n              =0.02) and basal microcirculatory resistance (mean [\n              <jats:styled-content style=\"fixed-case\">SD<\/jats:styled-content>\n              ], 76.3 [37.9] versus 55.4 [30.4] mm Hg\/s;\n              <jats:italic>P<\/jats:italic>\n              =0.02), whereas in controls, there was an increase in transit time (mean [SD], 0.48 [0.24] versus 0.83 [0.41] seconds;\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001) and basal microcirculatory resistance (mean [SD], 45.9 [34.7] versus 66.7 [37.2] mm Hg\/s;\n              <jats:italic>P<\/jats:italic>\n              =0.02).\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101R monoclonal antibody binding was confirmed in ventricular tissue but not in vascular tissue, and transmyocardial\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101 extraction was observed.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101 causes coronary microvascular dilation and increased flow but does not influence peripheral tone.\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101R immunohistochemistry suggests that\n              <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n              \u20101 coronary vasodilatation is indirectly mediated by ventricular\u2010coronary cross talk.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.118.010321","type":"journal-article","created":{"date-parts":[[2018,12,16]],"date-time":"2018-12-16T20:51:29Z","timestamp":1544993489000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":38,"title":["GLP\u20101 Is a Coronary Artery Vasodilator in Humans"],"prefix":"10.1161","volume":"7","author":[{"given":"Sophie J.","family":"Clarke","sequence":"first","affiliation":[{"name":"Division of Cardiovascular Medicine University of Cambridge United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joel P.","family":"Giblett","sequence":"additional","affiliation":[{"name":"Department of Interventional Cardiology Royal Papworth Hospital NHS Foundation Trust Cambridge United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucy L.","family":"Yang","sequence":"additional","affiliation":[{"name":"Division of Experimental Medicine and Immunotherapeutics University of Cambridge United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annette","family":"Hubsch","sequence":"additional","affiliation":[{"name":"Division of Experimental Medicine and Immunotherapeutics University of Cambridge United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tian","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Interventional Cardiology Royal Papworth Hospital NHS Foundation Trust Cambridge United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muhammad","family":"Aetesam\u2010ur\u2010Rahman","sequence":"additional","affiliation":[{"name":"Department of Interventional Cardiology Royal Papworth Hospital NHS Foundation Trust Cambridge United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nick E. 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