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The tachycardia induced by the stimulation of A\n                    <jats:sub>2A<\/jats:sub>\n                    or A\n                    <jats:sub>2B<\/jats:sub>\n                    receptors has been suggested to be mediated by a reflex increase in sympathetic activity. Here, we have investigated the role of \u03b2\n                    <jats:sub>1<\/jats:sub>\n                    \u2010 and \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010adrenoceptors in mediating the different cardiovascular responses to selective A\n                    <jats:sub>2A<\/jats:sub>\n                    and A\n                    <jats:sub>2B<\/jats:sub>\n                    receptor stimulation. Hemodynamic variables were measured in conscious male Sprague\u2010Dawley rats (350\u2013450\u00a0g) via pulsed Doppler flowmetry. The effect of intravenous infusion (3\u00a0min per dose) of the A\n                    <jats:sub>2A<\/jats:sub>\n                    \u2010selective agonist CGS 21680 (0.1, 0.3, 1.0\u00a0\u00b5g.kg\n                    <jats:sup>\u22121<\/jats:sup>\n                    .min\n                    <jats:sup>\u22121<\/jats:sup>\n                    ) or the A\n                    <jats:sub>2B<\/jats:sub>\n                    \u2010selective agonist BAY 60\u20136583 (4.0, 13.3, 40.0\u00a0\u00b5g.kg\n                    <jats:sup>\u22121<\/jats:sup>\n                    .min\n                    <jats:sup>\u22121<\/jats:sup>\n                    ) in the absence or following pre\u2010treatment with the non\u2010selective \u03b2\u2010antagonist propranolol (1.0\u00a0mg.kg\n                    <jats:sup>\u22121<\/jats:sup>\n                    ), the selective \u03b2\n                    <jats:sub>1<\/jats:sub>\n                    \u2010antagonist CGP 20712A (200\u00a0\u00b5g.kg\n                    <jats:sup>\u22121<\/jats:sup>\n                    ), or the selective \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010antagonist ICI 118,551 (2.0\u00a0mg.kg\n                    <jats:sup>\u22121<\/jats:sup>\n                    ) was investigated (maintenance doses also administered). CGP 20712A and propranolol significantly reduced the tachycardic response to CGS 21680, with no change in the effect on MAP. ICI 118,551 increased BAY 60\u20136583\u2010mediated renal and mesenteric flows, but did not affect the heart rate response. CGP 20712A attenuated the BAY 60\u20136583\u2010induced tachycardia. These data imply a direct stimulation of the sympathetic activity via cardiac \u03b2\n                    <jats:sub>1<\/jats:sub>\n                    \u2010adrenoceptors as a mechanism for the A\n                    <jats:sub>2A<\/jats:sub>\n                    \u2010 and A\n                    <jats:sub>2B<\/jats:sub>\n                    \u2010induced tachycardia. However, the regionally selective effects of A\n                    <jats:sub>2B<\/jats:sub>\n                    agonists on vascular conductance were independent of sympathetic activity and may be exploitable for the treatment of acute kidney injury and mesenteric ischemia.\n                  <\/jats:p>","DOI":"10.1002\/prp2.975","type":"journal-article","created":{"date-parts":[[2022,5,29]],"date-time":"2022-05-29T09:45:12Z","timestamp":1653817512000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Involvement of \u03b2\u2010adrenoceptors in the cardiovascular responses induced by selective adenosine A\n                    <sub>2A<\/sub>\n                    and A\n                    <sub>2B<\/sub>\n                    receptor agonists"],"prefix":"10.1002","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5489-0526","authenticated-orcid":false,"given":"Edward S.","family":"Wragg","sequence":"first","affiliation":[{"name":"Division of Physiology, Pharmacology and Neuroscience School of Life Sciences University of Nottingham  Nottingham UK"},{"name":"Centre of Membrane Proteins and Receptors University of Birmingham and University of Nottingham  Midlands UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1748-6911","authenticated-orcid":false,"given":"Patrizia","family":"Pannucci","sequence":"additional","affiliation":[{"name":"Division of Physiology, Pharmacology and Neuroscience School of Life Sciences University of Nottingham  Nottingham UK"},{"name":"Centre of Membrane Proteins and Receptors University of Birmingham and University of Nottingham  Midlands UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4424-239X","authenticated-orcid":false,"given":"Stephen J.","family":"Hill","sequence":"additional","affiliation":[{"name":"Division of Physiology, Pharmacology and Neuroscience School of Life Sciences University of Nottingham  Nottingham UK"},{"name":"Centre of Membrane Proteins and Receptors University of Birmingham and University of Nottingham  Midlands UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5406-6847","authenticated-orcid":false,"given":"Jeanette","family":"Woolard","sequence":"additional","affiliation":[{"name":"Division of Physiology, Pharmacology and Neuroscience School of Life Sciences University of Nottingham  Nottingham UK"},{"name":"Centre of Membrane Proteins and Receptors University of Birmingham and University of Nottingham  Midlands UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9062-5893","authenticated-orcid":false,"given":"Samantha L.","family":"Cooper","sequence":"additional","affiliation":[{"name":"Division of Physiology, Pharmacology and Neuroscience School of Life Sciences University of 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