原发性醛固酮增多症为发病率较高的继发性高血压且危害较大，有关发病机制尚不完全清楚。已有研究提示PCP4蛋白可通过调控钙调蛋白CaM和钙离子的结合和解离速度来调控钙离子水平达到调控醛固酮合成酶(CYP11B2)的表达，从而增加醛固酮合成。我们发现长链非编码RNA(lncRNA) uc003zpr.2的表达与PCP4表达相关并在原发性醛固酮增多症升高，体外过表达或沉默uc003zpr.2，PCP4和醛固酮合成酶mRNA和蛋白表达量出现增加或减少相应变化，故uc003zpr.2 可能在原发性醛固酮增多症形成中起重要作用。据此我们提出科学假设： uc003zpr.2通过靶分子上调PCP4和醛固酮合成酶基因的表达，促进醛固酮合成。本研究的目的就是探讨这些与uc003zpr.2结合蛋白或DNA或RNA序列，明确其调控PCP4的机理，进一步阐明原发性醛固酮增多症发病机制。

Primary aldosteronism（PA） is of high incidence in secondary hypertension，and the disease causes heavy damage. But the mechanism of the disease has not been fully revealed.Previous studies have shown that PCP4 could positively regulate the expression of aldosterone synthase(CYP11B2) and aldosterone secretion.This action of PCP4 is via regulating the intracellular calcium level by accelerating calcium association and dissociation with calmodulin(CaM). In our previous work,we have found that long non-coding RNA(lncRNA) uc003zpr.2 was specificially upregulated in the PA samples,and it was highly associated with the expression of PCP4.In H295R cells,Knocking down of lncRNA uc003zpr.2 decreased the PCP4 and aldosterone synthase(CYP11B2) expression levels,whereas overexpression of lncRNA uc003zpr.2 increased PCP4, aldosterone synthase(CYP11B2) levels and aldosterone production，these suggest that lncRNA uc003zpr.2 may play a key role in the primary aldosteronism. Based on theses findings,we hypothesize that lncRNA uc003zpr.2 may regulate the expression of PCP4 by combining a specific target gene or protein,and then increase the intracellular calcium, aldosterone synthase(CYP11B2) levels and aldosterone production.We plan to further detect the mechanism underlying the effect of lncRNA uc003zpr.2 on PCP4 expression,and explore the role of lncRNA uc003zpr.2 in the pathogenesis of primary aldosteronism.