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特发性醛固酮增多症(idiopathic hyperaldoste-ronism,IHA)和原发性低肾素型高血压(low-renin essential hypertension,LREH)是高血压的常见类型,以醛固酮肾素比值升高和对血管紧张素Ⅱ高度敏感为特征,它们是同一疾病中的两种状态,当肾素醛固酮系统控制醛固酮生成作用减弱时,可导致LREH进展为IHA。然而驱动该进程的机制尚不明确。在小鼠中,TWIK相关酸敏感钾离子通道(TWIK-related acid-sensitive K+channels,TASK)亚单位TASK-1和TASK-3缺失(T1T3KO)可产生人类IHA疾病模型。该研究探索当仅存在TASK-3缺失(T3KO)时,其对醛固酮分泌和血压
Idiopathic hyperaldoste-ronism (idiopathic hyperaldoste-ronism, IHA) and essential low-renin essential hypertension (LREH) are common types of hypertension, with increased aldosterone renin ratios and increased risk of vascular Tensin II is characterized by its high sensitivity. They are two states in the same disease. When the renin aldosterone system controls the aldosterone production weakened, it leads to the progression of LREH to IHA. However, the mechanism that drives this process is not yet clear. In mice, the TIKK-related acid-sensitive K + channels (TASK) subunits TASK-1 and TASK-3 deletion (T1T3KO) produce human IHA disease models. This study explored the role of aldosterone secretion and blood pressure in the presence of only TASK-3 deletion (T3KO)