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However, the role of <jats:styled-content style=\"fixed-case\">APJ<\/jats:styled-content> interaction with opioid receptors (<jats:styled-content style=\"fixed-case\">OPR<\/jats:styled-content>) on the cardiovascular effects of apelin in hypertension is not clear. Renovascular hypertension was induced by placing a Plexiglas clip on the left kidney of rats. After 16\u00a0weeks, F13A (an <jats:styled-content style=\"fixed-case\">APJ<\/jats:styled-content> antagonist), naloxone (a general <jats:styled-content style=\"fixed-case\">OPR<\/jats:styled-content> inhibitor), and nor\u2010binaltorphimine dihydrochloride (nor\u2010<jats:styled-content style=\"fixed-case\">BNI<\/jats:styled-content>; a selective inhibitor of <jats:styled-content style=\"fixed-case\">KOR<\/jats:styled-content>) were given prior to injections of apelin at doses of 40 and 60\u00a0\u03bcg\/kg. The arterial systolic\/diastolic blood pressure and left ventricular contractility responses were then evaluated. The arterial systolic\/diastolic blood pressure in sham and 2K1C rats was 110\/71\u00a0mm\u00a0Hg and 171\/124\u00a0mm\u00a0Hg, respectively. The hypotensive effects of apelin at both doses were inhibited by F13A and naloxone. Nor\u2010<jats:styled-content style=\"fixed-case\">BNI<\/jats:styled-content> completely inhibited the effects of apelin 40 on arterial pressure, and decreased the effects of 60\u00a0\u03bcg\/kg. <jats:styled-content style=\"fixed-case\">KOR<\/jats:styled-content> inhibition also prevented the compensation for the decrease in the left ventricle +dp\/dt max and \u2212dp\/dt max caused by apelin 60. The simultaneous inhibition of <jats:styled-content style=\"fixed-case\">OPR<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">APJ<\/jats:styled-content> reduced arterial pressure and increased cardiac contractility. Findings showed that the <jats:styled-content style=\"fixed-case\">OPR<\/jats:styled-content>, particularly <jats:styled-content style=\"fixed-case\">KOR<\/jats:styled-content>, mediate the inotropic, lusitropic, and depressor effects of apelin. The interaction of the <jats:styled-content style=\"fixed-case\">OPR<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">APJ<\/jats:styled-content> augments the inotropic and vasodepressor effects of apelin. This interaction may have potential clinical applications in cardiac failure since opioids are currently used in the treatment of myocardial infarction and stroke, and apelin has been introduced as a potential therapeutic agent in cardiovascular complications.<\/jats:p>","DOI":"10.1111\/1440-1681.12860","type":"journal-article","created":{"date-parts":[[2017,9,25]],"date-time":"2017-09-25T16:30:31Z","timestamp":1506357031000},"page":"187-197","source":"Crossref","is-referenced-by-count":12,"title":["Opioid receptors mediate inotropic and depressor effects of apelin in rats with 2K1C\u2010induced chronic renovascular hypertension"],"prefix":"10.1111","volume":"45","author":[{"given":"Farzaneh","family":"Rostamzadeh","sequence":"first","affiliation":[{"name":"Neuroscience Research Center Institute of Neuropharmacology and Department of Physiology and Pharmacology Kerman University of Medical Sciences  Kerman 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