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An established risk factor for developing cardiovascular disease is the absence of a blood pressure dip during the inactive period. The goal of the present study was to determine the effects of a high salt diet plus mineralocorticoid on <jats:styled-content style=\"fixed-case\">PER<\/jats:styled-content>1\u2010mediated blood pressure regulation in a salt\u2010resistant, normotensive mouse model, C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6J.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Blood pressure was measured using radiotelemetry. After control diet, wild\u2010type (<jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>) and <jats:italic>Per1<\/jats:italic> (<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content>) knockout mice were given a high salt diet (4% NaCl) and the long\u2010acting mineralocorticoid deoxycorticosterone pivalate. Blood pressure and activity rhythms were analysed to evaluate changes over time.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Blood pressure in <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice was not affected by a high salt diet plus mineralocorticoid. In contrast, <jats:italic>Per1 <\/jats:italic><jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> mice exhibited significantly increased mean arterial pressure (<jats:styled-content style=\"fixed-case\">MAP<\/jats:styled-content>) in response to a high salt diet plus mineralocorticoid. The inactive\/active phase ratio of <jats:styled-content style=\"fixed-case\">MAP<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice was unchanged by high salt plus mineralocorticoid treatment. Importantly, this treatment caused <jats:italic>Per1 <\/jats:italic><jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> mice to lose the expected decrease or \u2018dip\u2019 in blood pressure during the inactive compared to the active phase.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Loss of <jats:styled-content style=\"fixed-case\">PER<\/jats:styled-content>1 increased sensitivity to the high salt plus mineralocorticoid treatment. It also resulted in a non\u2010dipper phenotype in this model of salt\u2010sensitive hypertension and provides a unique model of non\u2010dipping. Together, these data support an important role for the circadian clock protein <jats:styled-content style=\"fixed-case\">PER<\/jats:styled-content>1 in the modulation of blood pressure in a high salt\/mineralocorticoid model of hypertension.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.12804","type":"journal-article","created":{"date-parts":[[2016,9,16]],"date-time":"2016-09-16T15:56:55Z","timestamp":1474041415000},"page":"72-82","source":"Crossref","is-referenced-by-count":77,"title":["Desoxycorticosterone pivalate\u2010salt treatment leads to non\u2010dipping hypertension in Per1 knockout mice"],"prefix":"10.1111","volume":"220","author":[{"given":"K.","family":"Solocinski","sequence":"first","affiliation":[{"name":"Department of Medicine University of Florida Gainesville FL USA"},{"name":"Department of Biochemistry and Molecular Biology University of Florida Gainesville FL USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Holzworth","sequence":"additional","affiliation":[{"name":"Department of Medicine University of Florida Gainesville FL USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"X.","family":"Wen","sequence":"additional","affiliation":[{"name":"Department of Medicine University of Florida Gainesville FL USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.\u2010Y.","family":"Cheng","sequence":"additional","affiliation":[{"name":"Department of Medicine University of Florida Gainesville FL USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I. 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