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Global signalling of \u03b21ARs up-regulates both the influx of Ca2+ through sarcolemmal L-type Ca2+ channels (LCCs) and the release of Ca2+ from the sarcoplasmic reticulum (SR) through the ryanodine receptors (RyRs). However, we recently found that \u03b22AR stimulation meditates \u2018offside compartmentalization\u2019, confining \u03b21AR signalling into subsarcolemmal nanodomains without reaching SR proteins. In the present study, we aim to investigate the new question, whether and how compartmentalized \u03b21AR signalling regulates cardiac E-C coupling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>By combining confocal Ca2+ imaging and patch-clamp techniques, we investigated the effects of compartmentalized \u03b2AR signalling on E-C coupling at both cellular and molecular levels. We found that simultaneous activation of \u03b22 and \u03b21ARs, in contrast to global signalling of \u03b21ARs, modulated neither the amplitude and spatiotemporal properties of Ca2+ sparks nor the kinetics of the RyR response to LCC Ca2+ sparklets. Nevertheless, by up-regulating LCC current, compartmentalized \u03b21AR signalling synchronized RyR Ca2+ release and increased the functional reserve (stability margin) of E-C coupling. In circumstances of briefer excitation durations or lower RyR responsivity, compartmentalized \u03b2AR signalling, by increasing the intensity of Ca2+ triggers, helped stabilize the performance of E-C coupling and enhanced the Ca2+ transient amplitude in failing heart cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Given that compartmentalized \u03b2AR signalling can be induced by stress-associated levels of catecholamines, our results revealed an important, yet unappreciated, heart regulation mechanism that is autoadaptive to varied stress conditions.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvaa013","type":"journal-article","created":{"date-parts":[[2020,1,30]],"date-time":"2020-01-30T15:10:07Z","timestamp":1580397007000},"page":"2069-2080","source":"Crossref","is-referenced-by-count":10,"title":["Compartmentalized \u03b21-adrenergic signalling synchronizes excitation\u2013contraction coupling without modulating individual Ca2+ sparks in healthy and hypertrophied cardiomyocytes"],"prefix":"10.1093","volume":"116","author":[{"given":"Hua-Qian","family":"Yang","sequence":"first","affiliation":[{"name":"State Key Laboratory of Membrane Biology, College of Life Sciences, Peking University, 5 Yiheyuan Rd, Beijing 100871, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0385-4370","authenticated-orcid":false,"given":"Peng","family":"Zhou","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Membrane Biology, College of Life Sciences, Peking University, 5 Yiheyuan Rd, Beijing 100871, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2391-3609","authenticated-orcid":false,"given":"Li-Peng","family":"Wang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Membrane Biology, College of Life 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