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A proposed mechanism for the Berecek phenomenon with implications for cardiovascular reprogramming

机译:Berecek现象的提出机制,具有对心血管重新编程的影响

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Berecek et?al reported in the 1990s that when spontaneously hypertensive rat (SHR) mating pairs were treated with captopril and the resulting pups were continued on the drug for 2 months followed by drug discontinuation, the pups did not develop full blown hypertension, and the cardiovascular structural changes associated with hypertension in SHR were mitigated. The offspring of the pups also displayed diminished hypertension and structural changes, suggesting that the drug therapy produced a heritable amelioration of the SHR phenotype. This observation is reviewed. The link between cellular renin angiotensin systems and epigenetic histone modification is explored, and a mechanism responsible for the observation is proposed. In any case, the observations of Berecek are sufficiently intriguing and biologically important to merit re-exploration and definitive explanation. Equally important is determining the role of renin angiotensin systems in epigenetic modification.
机译:Berecek et?Al在20世纪90年代报道,当自发性高血压大鼠(SHR)交配对被CaptoPril治疗,并将所得幼仔继续在药物上进行2个月,然后用药停止,幼崽未发生全面爆发的高血压,以及 减轻了与shR高血压相关的心血管结构变化。 幼崽的后代也显示出高血压和结构变化的减少,表明药物治疗产生了SHR表型的遗传性改善。 审查了这种观察。 探讨了细胞肾素血管紧张素系统和表观遗传组蛋白修饰之间的联系,提出了负责观察的机制。 无论如何,Berecek的观察是足够的兴趣和生物学上的重要性,以重新探索和明确的解释。 同样重要的是确定肾素血管紧张素系统在表观遗传修饰中的作用。

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