1 ion in diagnosis and estimated prevalence of primary hyperaldosteronism.

2 osterone-producing adenomas of patients with primary hyperaldosteronism.

3 hannels as a possible therapeutic target for primary hyperaldosteronism.

4 annel knockout mice exhibit the hallmarks of primary hyperaldosteronism.

5 nsion including a large, undiagnosed pool of primary hyperaldosteronism.

6  establish an animal model of nontumorigenic primary hyperaldosteronism and identify TASK channels as

7 rmation of, and differentiation of causes of primary hyperaldosteronism and the Cushing syndrome.

8  11.8 years (range 28-69 years) diagnosed as primary hyperaldosteronism, and who underwent AVS from J

9          Yet, the etiology of nontumorigenic primary hyperaldosteronism caused by bilateral idiopathi

10 ese tumors cause endocrine diseases (such as primary hyperaldosteronism, hypercortisolism, hyperandro

11                                              Primary hyperaldosteronism is a well-recognized cause of

12                                              Primary hyperaldosteronism is an uncommon cause of hyper

13 se this result differs from that expected in primary hyperaldosteronism, our finding argues against l

14 ositron emission tomography in patients with primary hyperaldosteronism (PHA).

15 ic and germline mutations in ion channels in primary hyperaldosteronism underscores the importance of

16 3 blockade may offer a novel way of treating primary hyperaldosteronism, which avoids the vascular si

17 nge, 14-67 years; median age, 46 years) with primary hyperaldosteronism who underwent 1.5-T MR imagin