首页> 外文期刊>Japanese Journal of Pharmacology >Cardiac Hypertrophy-Related Gene Expression in Spontaneously Hypertensive Rats: Crucial Role of Angiotensin AT1, Receptor
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Cardiac Hypertrophy-Related Gene Expression in Spontaneously Hypertensive Rats: Crucial Role of Angiotensin AT1, Receptor

机译:自发性高血压大鼠心脏肥大相关基因表达:血管紧张素AT1,受体的关键作用。

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References(16) Cited-By(6) Angiotensin converting-enzyme inhibitors (alacepril and imidapril) or an AT1, -receptor antagonist (SC-52458) was administered to 10-week-old spontaneously hypertensive rats (SHR) for 7 days, and cardiac mRNA levels for contractile proteins and atrial natriuretic polypeptide (ANP) were comprehensively measured. The expression of skeletal α-actin and ANP was selectively enhanced in the heart of vehicle-treated SHR compared with Wistar-Kyoto rats (WKY), thereby suggesting that the phenotypic modulation of myocytes occurred at the early stage of hypertension. The above-mentioned three drugs similarly suppressed these enhanced gene expressions, nearly to the control levels. In contrast, although the treatment with hydralazine lowered the blood pressure of SHR similarly, hydralazine did not suppress ANP expression at all and only partially suppressed skeletal α-actin. Moreover, alacepril did not affect these gene expressions in WKY. Thus, AT1, receptor may be crucial for phenotypic modulation in the heart of SHR.
机译:参考文献(16)被引用的(6)血管紧张素转化酶抑制剂(阿那普利和咪哒普利)或AT1受体拮抗剂(SC-52458)被给予10周大的自发性高血压大鼠(SHR),持续7天,全面测量心脏收缩蛋白和心钠素的mRNA水平。与Wistar-Kyoto大鼠(WKY)相比,用载体治疗的SHR的心脏中选择性增强了骨骼肌α-肌动蛋白和ANP的表达,从而表明心肌细胞的表型调节发生在高血压的早期。上述三种药物类似地抑制了这些增强的基因表达,几乎达到了对照水平。相反,尽管肼屈嗪的治疗类似地降低了SHR的血压,但是肼屈嗪根本不抑制ANP表达,而仅部分抑制骨骼肌α-肌动蛋白。而且,alacepril不会影响WKY中的这些基因表达。因此,AT1受体可能对SHR心脏的表型调节至关重要。

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