@article {Rostamzadeh:2018:0305-1870:187,
title = "Opioid receptors mediate inotropic and depressor effects of apelin in rats with 2K1Cinduced chronic renovascular hypertension",
journal = "Clinical and Experimental Pharmacology and Physiology",
parent_itemid = "infobike://bsc/cep",
publishercode ="bp",
year = "2018",
volume = "45",
number = "2",
publication date ="2018-02-01T00:00:00",
pages = "187-197",
itemtype = "ARTICLE",
issn = "0305-1870",
eissn = "1440-1681",
url = "https://www.ingentaconnect.com/content/bsc/cep/2018/00000045/00000002/art00010",
doi = "doi:10.1111/1440-1681.12860",
keyword = "myocardial contractility, apelin receptors, kappa opioid receptors, receptor interaction, renovascular hypertension",
author = "Rostamzadeh, Farzaneh and Najafipour, Hamid and YeganehHajahmadi, Mahboobeh and Joukar, Siyavash",
abstract = "Apelin receptors (APJ) crosstalk with other Gproteincoupled receptors. However, the role of APJ interaction with opioid receptors (OPR) 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 16weeks, F13A (an APJ antagonist), naloxone (a general OPR inhibitor), and norbinaltorphimine dihydrochloride (norBNI; a selective inhibitor of KOR) were given prior to injections of apelin at doses of 40 and 60g/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 110/71mmHg and 171/124mmHg, respectively. The hypotensive effects of apelin at both
doses were inhibited by F13A and naloxone. NorBNI completely inhibited the effects of apelin 40 on arterial pressure, and decreased the effects of 60g/kg. KOR inhibition also prevented the compensation for the decrease in the left ventricle +dp/dt max and dp/dt max
caused by apelin 60. The simultaneous inhibition of OPR and APJ reduced arterial pressure and increased cardiac contractility. Findings showed that the OPR, particularly KOR, mediate the inotropic, lusitropic, and depressor effects of apelin. The interaction of the OPR and APJ 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.",
}