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The aim of this study was to elucidate the mechanisms underlying this abnormality.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Male Sprague Dawley rats received either chow containing adenine or were pair\u2010fed with normal chow (controls). After 8\u201314\u00a0weeks, arterial function was analysed <jats:italic>ex\u00a0vivo<\/jats:italic> using wire myography and the expression of proteins involved in vascular smooth muscle excitation\u2013contraction coupling in the thoracic aorta was analysed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The rate of relaxation following washout of <jats:styled-content style=\"fixed-case\">KC<\/jats:styled-content>l was reduced in A\u2010<jats:styled-content style=\"fixed-case\">CRF<\/jats:styled-content> rats vs. controls in the thoracic aorta (<jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.01), abdominal aorta (<jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.05), and common carotid artery (<jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.05), but not in the common femoral artery. Relaxation rates of thoracic aortas increased (<jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.01), but were not normalized, in response to washout of <jats:styled-content style=\"fixed-case\">KC<\/jats:styled-content>l with Ca<jats:sup>2+<\/jats:sup>\u2010free buffer. Microarray and <jats:styled-content style=\"fixed-case\">qRT<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content> analyses of genes involved in excitation\u2013contraction coupling identified 10 genes, which showed significantly altered expression in A\u2010<jats:styled-content style=\"fixed-case\">CRF<\/jats:styled-content> thoracic aortas. At the protein level, the <jats:italic>\u03b1<\/jats:italic>2 subunit of the Na,K\u2010<jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>ase (<jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.001) and <jats:styled-content style=\"fixed-case\">SERCA<\/jats:styled-content>2 (<jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.05) was significantly downregulated, whereas stromal interaction molecule 1 and calsequestrin\u20101 and calsequestrin\u20102 were significantly upregulated (<jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.05).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Rats with A\u2010<jats:styled-content style=\"fixed-case\">CRF<\/jats:styled-content> show a marked alteration in relaxation of larger conduit arteries localized proximal to the common femoral artery. This abnormality may be caused by reduced cytosolic Ca<jats:sup>2+<\/jats:sup> clearance in vascular smooth muscle cells secondary to dysregulation of proteins crucially involved in this process.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.12724","type":"journal-article","created":{"date-parts":[[2016,5,30]],"date-time":"2016-05-30T13:32:48Z","timestamp":1464615168000},"page":"250-264","source":"Crossref","is-referenced-by-count":9,"title":["Adenine\u2010induced chronic renal failure in rats decreases aortic relaxation rate and alters expression of proteins involved in vascular smooth muscle calcium handling"],"prefix":"10.1111","volume":"218","author":[{"given":"L.","family":"Nguy","sequence":"first","affiliation":[{"name":"Department of Molecular and Clinical Medicine\/Nephrology Institute of Medicine Gothenburg Sweden"},{"name":"Department of Physiology Institute of Neuroscience and Physiology Gothenburg 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