| [1] |
Seccia TM, Caroccia B, Gomez-Sanchez EP, et al. The biology of normal zona glomerulosa and aldosterone-producing adenoma: pathological implications[J]. Endocr Rev, 2018, 39:1029-1056.
|
| [2] |
Hu C, Rusin CG, Tan Z, et al. Zona glomerulosa cells of the mouse adrenal cortex are intrinsic electrical oscillators[J]. J Clin Invest, 2012, 122:2046-2053.
|
| [3] |
Leng S, Pignatti E, Khetani RS, et al. β-catenin and FGFR2 regulate postnatal rosette-based adrenocortical morphogenesis[J]. Nat Commun, 2020, 11:1680. doi: 10.1038/s41467-020-15332-7.
|
| [4] |
Zhu Y, Zhang X, Hu C. Structure of rosettes in the zona glomerulosa of human adrenal cortex[J]. J Anat, 2023, 243:684-689.
|
| [5] |
Guagliardo NA, Klein PM, Gancayco CA, et al. Angiotensin Ⅱ induces coordinated calcium bursts in aldosterone-producing adrenal rosettes[J]. Nat Commun, 2020, 11:1679. doi: 10.1038/s41467-020-15408-4.
|
| [6] |
Guagliardo NA, Yao J, Hu C, et al. TASK-3 channel deletion in mice recapitulates low-renin essential hypertension[J]. Hypertension, 2012, 59:999-1005.
|
| [7] |
Lee BC, Kang VJ, Pan CT, et al. KCNJ5 somatic mutation is associated with higher aortic wall thickness and less calcification in patients with aldosterone-producing adenoma[J]. Front Endocrinol (Lausanne), 2022, 13:830130.doi:10.3389/fendo.2022.830130.
|
| [8] |
Chang YY, Lee BC, Chen ZW, et al. Cardiovascular and metabolic characters of KCNJ5 somatic mutations in primary aldosteronism[J]. Front Endocrinol (Lausanne), 2023, 14:1061704.
|
| [9] |
Enyeart JJ, Enyeart JA. Human adrenal glomerulosa cells express K2P and GIRK potassium channels that are inhibited by ANG Ⅱ and ACTH[J]. Am J Physiol Cell Physiol, 2021, 321:C158-C175.
|
| [10] |
Guagliardo NA, Yao J, Stipes EJ, et al. Adrenal tissue-specific deletion of TASK channels causes aldosterone-driven angiotensin Ⅱ-independent hypertension[J]. Hypertension, 2019, 73:407-414.
|
| [11] |
Gancayco CA, Gerding MR, Breault DT, et al. Ntrinsic adrenal TWIK-related acid-sensitive TASK channel dysfunction produces spontaneous calcium oscillations sufficient to drive AngⅡ (Angiotensin Ⅱ)-unresponsive hyperaldosteronism[J]. Hypertension, 2022, 79:2552-2564.
|
| [12] |
Chen AX, Nishimoto K, Nanba K, et al. Potassium channels related to primary aldosteronism: expression similarities and differences between human and rat adrenals[J]. Mol Cell Endocrinol, 2015, 417:141-148.
|
| [13] |
Manichaikul A, Rich SS, Allison MA, et al. KCNK3 variants are associated with hyperaldosteronism and hypertension[J]. Hypertension, 2016, 68:356-364.
|
| [14] |
Arrighi I, Bloch-Faure M, Grahammer F, et al. Altered potassium balance and aldosterone secretion in a mouse model of human congenital long QT syndrome[J]. PNAS, 2001, 98:8792-8797.
|
| [15] |
Yang T, Zhang H, Liang Q, et al. Small-conductance Ca2+-activated potassium channels negatively regulate aldosterone secretion in human adrenocortical cells[J]. Hypertension, 2016, 68:785-795.
|
| [16] |
Grimm PR, Irsik DL, Settles DC, et al. Hypertension of Kcnmb1-/- is linked to deficient K secretion and aldosteronism[J]. PNAS, 2009, 106:11800-11805.
|
| [17] |
Larsen CK, Jensen IS, Sorensen MV, et al. Hyperaldosteronism after decreased renal K+excretion in KCNMB2 knockout mice[J]. Am J Physiol Renal Physiol, 2016, 310:F1035-F1046.
|
| [18] |
Cornelius RJ, Wen D, Hatcher LI, et al. Bicarbonate promotes BK-α/β4-mediated K excretion in the renal distal nephron[J]. Am J Physiol Renal Physiol, 2012, 303:F1563-F1571.
|
| [19] |
Rossier MF. T-type calcium channel: A privileged gate for calcium entry and control of adrenal steroidogenesis[J]. Front Endocrinol (Lausanne), 2016, 7:43. doi: 10.3389/fendo.2016.00043
|
| [20] |
Barrett PQ, Ertel EA, Smith MM, et al. Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone[J]. Am J Physiol, 1995, 268:C985-C992.
|
| [21] |
Yang T, He M, Hu C, et al. L- and T-type calcium channels control aldosterone production from human adrenals[J]. J Endocrinol, 2020, 244:237-247.
|
| [22] |
Perez-Reyes E. Molecular physiology of low-voltage-activated T-type calcium channels[J]. Physiol Rev, 2003, 83:117-161.
|
| [23] |
Scholl UI, Goh G, Stölting G, et al. Somatic and germline CACNA1D calcium channel mutations in aldosterone-producing adenomas and primary aldosteronism[J]. Nature Genetics, 2013, 45:1050-1054.
|
| [24] |
Scholl UI, Stölting G, Schewe J, et al. CLCN2 chloride channel mutations in familial hyperaldosteronism type Ⅱ[J]. Nature Genetics, 2018, 50:349-354.
|
| [25] |
Fernandes-Rosa FL, Daniil G, Orozco IJ, et al. A gain-of-function mutation in the CLCN2 chloride channel gene causes primary aldosteronism.[J]. Nat Genet., 2018, 50:355-361.
|
