{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T13:36:22Z","timestamp":1790516182068,"version":"4.1.0"},"reference-count":29,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2018,7,11]],"date-time":"2018-07-11T00:00:00Z","timestamp":1531267200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["PG\/11\/45\/28975"],"award-info":[{"award-number":["PG\/11\/45\/28975"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acta Physiologica"],"published-print":{"date-parts":[[2018,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Aim<\/jats:title><jats:p>Hypoxia causes vasodilatation of coronary arteries which protects the heart from ischaemic damage through mechanisms including the generation of hydrogen sulphide (H<jats:sub>2<\/jats:sub>S), but the influence of the perivascular adipose tissue (<jats:styled-content style=\"fixed-case\">PVAT<\/jats:styled-content>) and myocardium is incompletely understood. This study aimed to determine whether <jats:styled-content style=\"fixed-case\">PVAT<\/jats:styled-content> and the myocardium modulate the coronary artery hypoxic response and whether this involves hydrogen sulphide.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Porcine left circumflex coronary arteries were prepared as cleaned segments and with <jats:styled-content style=\"fixed-case\">PVAT<\/jats:styled-content> intact, myocardium intact or both <jats:styled-content style=\"fixed-case\">PVAT<\/jats:styled-content> and myocardium intact, and contractility investigated using isometric tension recording. Immunoblotting was used to measure levels of H<jats:sub>2<\/jats:sub>S\u2010synthesizing enzymes: cystathionine\u2010\u03b2\u2010synthase (<jats:styled-content style=\"fixed-case\">CBS<\/jats:styled-content>), cystathionine \u03b3\u2010lyase (<jats:styled-content style=\"fixed-case\">CSE<\/jats:styled-content>) and 3\u2010mercaptopyruvate sulphurtransferase (<jats:styled-content style=\"fixed-case\">MPST<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>All three H<jats:sub>2<\/jats:sub>S\u2010synthesizing enzymes were detected in the artery and myocardium, but only <jats:styled-content style=\"fixed-case\">CBS<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">MPST<\/jats:styled-content> were detected in <jats:styled-content style=\"fixed-case\">PVAT<\/jats:styled-content>. Hypoxia elicited a biphasic response in cleaned artery segments consisting of transient contraction followed by prolonged relaxation. In arteries with <jats:styled-content style=\"fixed-case\">PVAT<\/jats:styled-content> intact, hypoxic contraction was attenuated and relaxation augmented. In arteries with myocardium intact, hypoxic contraction was attenuated, but relaxation was unaffected. In replacement experiments, replacement of dissected <jats:styled-content style=\"fixed-case\">PVAT<\/jats:styled-content> and myocardium attenuated artery contraction and augmented relaxation to hypoxia, mimicking the effect of in\u00a0situ <jats:styled-content style=\"fixed-case\">PVAT<\/jats:styled-content> and indicating involvement of a diffusible factor(s). In arteries with intact <jats:styled-content style=\"fixed-case\">PVAT<\/jats:styled-content>, augmentation of hypoxic relaxation was reversed by amino\u2010oxyacetate (<jats:styled-content style=\"fixed-case\">CBS<\/jats:styled-content> inhibitor), but not <jats:styled-content style=\"fixed-case\">DL<\/jats:styled-content>\u2010propargylglycine (<jats:styled-content style=\"fixed-case\">CSE<\/jats:styled-content> inhibitor) or aspartate (inhibits <jats:styled-content style=\"fixed-case\">MPST<\/jats:styled-content> pathway).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">PVAT<\/jats:styled-content> augments hypoxic relaxation of coronary arteries through a mechanism involving H<jats:sub>2<\/jats:sub>S and <jats:styled-content style=\"fixed-case\">CBS<\/jats:styled-content>, pointing to an important role in regulation of coronary blood flow during hypoxia.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.13126","type":"journal-article","created":{"date-parts":[[2018,6,13]],"date-time":"2018-06-13T08:25:08Z","timestamp":1528878308000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Coronary artery hypoxic vasorelaxation is augmented by perivascular adipose tissue through a mechanism involving hydrogen sulphide and cystathionine\u2010\u03b2\u2010synthase"],"prefix":"10.1111","volume":"224","author":[{"given":"J.","family":"Donovan","sequence":"first","affiliation":[{"name":"School of Life Sciences University of Nottingham Nottingham UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7051-0573","authenticated-orcid":false,"given":"P. 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