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首页> 外文期刊>Life sciences >Heterodimerization of apelin and opioid receptors and cardiac inotropic and lusitropic effects of apelin in 2K1C hypertension: Role of pERK1/2 and PKC
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Heterodimerization of apelin and opioid receptors and cardiac inotropic and lusitropic effects of apelin in 2K1C hypertension: Role of pERK1/2 and PKC

机译：阿糖素和阿片类药物的异素化和Apelin在2K1C高血压中的心肌肌室和疏水性效应：PERK1 / 2和PKC的作用

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Abstract Aims Kappa Opioid receptors (KORs) change the impact of apelin on the phosphorylated ERK1/2 (pERK1/2). However, the role of interaction between KOR and apelin receptors (APJ) on the cardiac contractility effects of apelin and in regulation of pERK1/2 and PKC in the heart of renovascular hypertensive (2K1C) rats is unknown. Main methods Hemodynamic factors, the heterodimerization of KOR and APJ, the expression of KOR mRNA and protein and pERK1/2 in the left ventricle of 2K1C rats were measured following APJ, KOR, PKC and Gi path inhibition by F13A, nor-BNI, chelerythrine and PTX respectively. Key findings Apelin in 40 and 60μg/kg doses increased cardiac contractility, and reduced mean arterial pressure. The cardiac impacts in both doses were reduced by F13A, nor-BNI and chelerytrine and blocked by PTX. Hypertension increased the expression of KORs and heterodimerization of APJ and KOR, and reduced pERK1/2 in the left ventricle. Apelin, in both doses reduced (normalized) heterodimerization and recovered the reduction in pERK1/2. The recovery of ERK1/2 phosphorylation was accompanied by reduction of KOR and APJ heterodimerization. Significance 2K1C hypertension increased the expression of KORs and heterodimerization of APJ and KORs. The heterodimerization was associated by reduction of ERK phosphorylation and altered the cardiac inotropic and lusitropic effects of apelin. These changes may participate in pathophysiology of cardiac dysfunction in renovascular hypertension that is associated with subnormal level of serum apelin. Apelin- induced recovery of ERK1/2 phosphorylation and KOR-APJ dimerization may nominate apelin as a therapeutic goal in treatment of this kind of hypertension.
机译：摘要AIMS Kappa ApioID受体（KORS）改变阿贝林对磷酸化ERK1 / 2（PERK1 / 2）的影响。然而，KOR和APELIN受体（APJ）之间的相互作用在血管内高血压（2K1C）大鼠心脏的心脏收缩性和PKC中的心脏收缩效应上的作用是未知的。主要方法血液动力学因素，KOR和APJ的异二聚体，在APJ，Kor，PKC和GI抑制作用2K1C大鼠左心室中KOR mRNA和蛋白质和PERK1 / 2的表达，C13A，NOR-BNI，Chelerythrine和PTX分别。键发现40〜60μg/ kg / kg剂量增加的心脏收缩力，平均动脉压力降低。通过F13A，NOR-BNI和CHELERYTRINE减少了两种剂量中的心脏撞击，并被PTX封闭。高血压提高了APJ和KOR的kors和异二聚体的表达，并在左心室中减少了perk1 / 2。 Apelin，两种剂量减少（归一化）异二聚体并回收了Perk1 / 2的还原。 ERK1 / 2磷酸化的回收伴随着kor和APJ异二聚体的减少。意义2k1C高血压增加了APJ和KORS的KOR和异二聚体的表达。异二聚体通过降低ERK磷酸化并改变阿蛋白的心脏尿体和疏水效应。这些变化可以参与肾血管性高血压中心脏功能障碍的病理生理学，其与血清素蛋白的亚肠道水平相关。 Enelin-诱导的ERK1 / 2磷酸化回收和KOR-APJ二聚化可以根据治疗这种高血压的治疗目标提名。

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