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首页> 外文期刊>Cellular Physiology and Biochemistry >Influence of atenolol and nifedipine on nitric-oxide deficient cardiomyocyte hypertrophy and expression of the cardio-endocrine peptide intermedin and its receptor components
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Influence of atenolol and nifedipine on nitric-oxide deficient cardiomyocyte hypertrophy and expression of the cardio-endocrine peptide intermedin and its receptor components

机译：阿替洛尔和硝苯地平对一氧化氮缺乏型心肌细胞肥大及心内分泌肽中介素及其受体成分的影响

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Background/aims: Chronic inhibition of nitric oxide ( NO) synthesis is associated with hypertension, myocardial ischemia, oxidative stress and hypertrophy; expression of adrenomedullin ( AM) and intermedin (IMD) and their receptor activity modifying proteins (RAMPs 1-3) is augmented in cardiomyocytes, indicating that the myocardial AM/IMD system may be activated in response to pressure loading and ischemic insult. The aim was to examine effects on (i) parameters of cardiomyocyte hypertrophy and on (ii) expression of AM and IMD and their receptor components in NO-deficient cardiomyocytes of an intervention chosen specifically for ability to alleviate pressure loading and ischemic injury concurrently. Methods: The NO synthesis inhibitor, N-G-nitro-L-arginine methyl ester (L-NAME, 35mg. kg(-1). day(-1)) was given to rats for 8 weeks, with/without concurrent administration of beta-adrenoceptor antagonist, atenolol ( 25mg. kg(-1). day(-1)) / calcium channel blocker, nifedipine (20mg. kg(-1). day(-1)). Results: In L-NAME treated rats, atenolol / nifedipine abolished increases in systolic blood pressure and plasma AM and IMD levels and in left ventricular cardiomyocytes: (i) normalized increased cell width and mRNA expression of hypertrophic (sk-alpha-actin) and cardio-endocrine (ANP, BNP, ET) genes; (ii) normalized augmented membrane protein oxidation; (iii) normalized mRNA expression of AM, IMD, RAMP1, RAMP2 and RAMP3. Conclusions: normalization of blood pressure and membrane oxidant status together with prevention of hypertrophy and normalization of the augmented expression of AM, IMD and their receptor components in NO-deficient cardiomyocytes by atenolol / nifedipine supports involvement of both pressure loading and ischemic insult in stimulating cardiomyocyte hypertrophy and induction of these counter-regulatory peptides and their receptor components. Attenuation of augmented expression of IMD in this model cannot however be explained simply by prevention of cardiomyocyte hypertrophy. Copyright (c) 2008 S. Karger AG, Basel.
机译：背景/目的：慢性抑制一氧化氮（NO）的合成与高血压，心肌缺血，氧化应激和肥大有关。心肌细胞中肾上腺髓质素（AM）和间质素（IMD）的表达及其受体活性修饰蛋白（RAMPs 1-3）增强，表明心肌AM / IMD系统可响应压力负荷和缺血性损伤而被激活。目的是研究对（NO）缺氧性心肌细胞中（i）心肌肥大参数和（ii）AM和IMD及其受体成分的表达的影响，该干预是专门为缓解压力负荷和缺血性损伤的能力而专门选择的。方法：将NO合成抑制剂NG-硝基-L-精氨酸甲酯（L-NAME，35mg。kg（-1）.day（-1））给予大鼠8周，有/无同时服用β -肾上腺素受体拮抗剂，阿替洛尔（25mg。kg（-1）.day（-1））/钙通道阻滞剂，硝苯地平（20mg.kg（-1）.day（-1））。结果：在接受L-NAME治疗的大鼠中，阿替洛尔/硝苯地平消除了收缩压，血浆AM和IMD水平以及左室心肌细胞的升高：（i）肥大性（sk-alpha-actin）和心脏内分泌（ANP，BNP，ET）基因; （ii）标准化的增强膜蛋白氧化; （iii）AM，IMD，RAMP1，RAMP2和RAMP3的mRNA标准化表达。结论：阿替洛尔/硝苯地平使血压和膜氧化状态正常化，并防止肥大和使NO缺乏型心肌细胞中AM，IMD及其受体成分的表达正常化，支持压力负荷和缺血性损伤均参与刺激心肌细胞这些反调节肽及其受体成分的肥大和诱导。但是，不能通过预防心肌肥大简单地解释该模型中IMD增强表达的减弱。版权所有（c）2008 S. Karger AG，巴塞尔。

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