دورية أكاديمية
أعرض في EDS

Human adrenal glomerulosa cells express K2P and GIRK potassium channels that are inhibited by ANG II and ACTH.

التفاصيل البيبلوغرافية
العنوان: Human adrenal glomerulosa cells express K2P and GIRK potassium channels that are inhibited by ANG II and ACTH.
المؤلفون: Enyeart JJ; Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, Ohio., Enyeart JA; Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, Ohio.
المصدر: American journal of physiology. Cell physiology [Am J Physiol Cell Physiol] 2021 Jul 01; Vol. 321 (1), pp. C158-C175. Date of Electronic Publication: 2021 May 26.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: American Physiological Society Country of Publication: United States NLM ID: 100901225 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1522-1563 (Electronic) Linking ISSN: 03636143 NLM ISO Abbreviation: Am J Physiol Cell Physiol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Bethesda, Md. : American Physiological Society,
مواضيع طبية MeSH: Adrenocorticotropic Hormone/*pharmacology , Angiotensin II/*pharmacology , G Protein-Coupled Inwardly-Rectifying Potassium Channels/*genetics , Kv1.4 Potassium Channel/*genetics , Nerve Tissue Proteins/*genetics , Potassium Channels, Tandem Pore Domain/*genetics , Zona Glomerulosa/*metabolism, Adolescent ; Adult ; Aldosterone/biosynthesis ; Arachidonic Acid/pharmacology ; Autopsy ; Child ; Colforsin/pharmacology ; Female ; G Protein-Coupled Inwardly-Rectifying Potassium Channels/metabolism ; Gene Expression ; Humans ; Kv1.4 Potassium Channel/antagonists & inhibitors ; Kv1.4 Potassium Channel/metabolism ; Male ; Membrane Potentials/drug effects ; Membrane Potentials/physiology ; Middle Aged ; Nerve Tissue Proteins/antagonists & inhibitors ; Nerve Tissue Proteins/metabolism ; Patch-Clamp Techniques ; Potassium Channels, Tandem Pore Domain/antagonists & inhibitors ; Potassium Channels, Tandem Pore Domain/metabolism ; Primary Cell Culture ; Zona Glomerulosa/cytology ; Zona Glomerulosa/drug effects
مستخلص: In whole cell patch clamp recordings, it was discovered that normal human adrenal zona glomerulosa (AZG) cells express members of the three major families of K + channels. Among these are a two-pore (K2P) leak-type and a G protein-coupled, inwardly rectifying (GIRK) channel, both inhibited by peptide hormones that stimulate aldosterone secretion. The K2P current displayed properties identifying it as TREK-1 (KCNK2). This outwardly rectifying current was activated by arachidonic acid and inhibited by angiotensin II (ANG II), adrenocorticotrophic hormone (ACTH), and forskolin. The activation and inhibition of TREK-1 was coupled to AZG cell hyperpolarization and depolarization, respectively. A second K2P channel, TASK-1 (KCNK3), was expressed at a lower density in AZG cells. Human AZG cells also express inwardly rectifying K + current(s) (K IR ) that include quasi-instantaneous and time-dependent components. This is the first report demonstrating the presence of K IR in whole cell recordings from AZG cells of any species. The time-dependent current was selectively inhibited by ANG II, and ACTH, identifying it as a G protein-coupled (GIRK) channel, most likely K IR 3.4 (KCNJ5). The quasi-instantaneous K IR current was not inhibited by ANG II or ACTH and may be a separate non-GIRK current. Finally, AZG cells express a voltage-gated, rapidly inactivating K + current whose properties identified as K V 1.4 (KCNA4), a conclusion confirmed by Northern blot. These findings demonstrate that human AZG cells express K2P and GIRK channels whose inhibition by ANG II and ACTH is likely coupled to depolarization-dependent secretion. They further demonstrate that human AZG K + channels differ fundamentally from the widely adopted rodent models for human aldosterone secretion.
References: Biochemistry. 1999 Oct 26;38(43):14286-93. (PMID: 10572003)
J Steroid Biochem Mol Biol. 2004 Oct;92(3):209-18. (PMID: 15555914)
J Membr Biol. 2003 Oct 1;195(3):147-64. (PMID: 14724761)
Physiol Rev. 2010 Apr;90(2):559-605. (PMID: 20393194)
J Biol Chem. 2000 Nov 3;275(44):34640-9. (PMID: 10913143)
J Biol Chem. 2005 Sep 2;280(35):30814-28. (PMID: 15994319)
Mol Endocrinol. 2006 May;20(5):953-70. (PMID: 16141358)
J Gen Physiol. 2008 Aug;132(2):279-94. (PMID: 18663135)
Endocrinology. 1987 Mar;120(3):903-14. (PMID: 3803318)
Heart Fail Rev. 2005 Jan;10(1):7-13. (PMID: 15947886)
Am J Physiol. 1979 Aug;237(2):E158-62. (PMID: 464092)
Mol Endocrinol. 1993 Aug;7(8):1031-40. (PMID: 8232302)
Am J Physiol. 1992 Oct;263(4 Pt 1):E752-9. (PMID: 1415696)
J Biol Chem. 1993 Apr 25;268(12):8640-4. (PMID: 8386167)
Nat Commun. 2014 Nov 25;5:5540. (PMID: 25420509)
Pflugers Arch. 2015 May;467(5):1027-42. (PMID: 25339223)
Endocrinology. 1993 Oct;133(4):1555-61. (PMID: 8404594)
Science. 2011 Feb 11;331(6018):768-72. (PMID: 21311022)
J Physiol Pharmacol. 2012 Oct;63(5):457-62. (PMID: 23211299)
Physiol Rev. 2010 Jan;90(1):291-366. (PMID: 20086079)
Science. 1998 Dec 18;282(5397):2275-9. (PMID: 9856955)
Nat Rev Neurosci. 2010 May;11(5):301-15. (PMID: 20389305)
Nature. 1998 Feb 19;391(6669):803-6. (PMID: 9486652)
Mol Cell Endocrinol. 2015 Dec 5;417:141-8. (PMID: 26375812)
Endocrinology. 1987 Apr;120(4):1581-9. (PMID: 3830061)
J Gen Physiol. 1993 Aug;102(2):239-55. (PMID: 8228910)
J Gen Physiol. 2013 Aug;142(2):137-55. (PMID: 23858003)
Mol Pharmacol. 2004 Mar;65(3):599-610. (PMID: 14978238)
Endocrinology. 1994 Jun;134(6):2589-98. (PMID: 7515004)
J Clin Endocrinol Metab. 2012 Aug;97(8):E1567-72. (PMID: 22628608)
J Physiol. 2016 Oct 15;594(20):5851-5860. (PMID: 26845064)
J Biol Chem. 2011 Apr 22;286(16):13977-84. (PMID: 21362619)
Mol Endocrinol. 2000 Jun;14(6):863-74. (PMID: 10847588)
J Biol Chem. 1999 Jan 22;274(4):2571-82. (PMID: 9891030)
Pflugers Arch. 1981 Aug;391(2):85-100. (PMID: 6270629)
Mol Endocrinol. 2002 Mar;16(3):621-9. (PMID: 11875121)
Elife. 2016 Apr 13;5:. (PMID: 27074664)
Mol Cell Endocrinol. 2012 Mar 24;350(2):151-62. (PMID: 21839803)
Am J Physiol Cell Physiol. 2007 Aug;293(2):C682-95. (PMID: 17494631)
J Gen Physiol. 1993 Aug;102(2):217-37. (PMID: 8228909)
Nature. 1998 Dec 3;396(6710):474-7. (PMID: 9853756)
Nature. 1995 Mar 9;374(6518):135-41. (PMID: 7877685)
Endocrinology. 2017 Feb 1;158(2):239-251. (PMID: 27901589)
J Biol Chem. 2002 Dec 20;277(51):49186-99. (PMID: 12368289)
Mol Pharmacol. 2003 Jul;64(1):132-42. (PMID: 12815169)
EMBO J. 2012 Aug 1;31(15):3297-308. (PMID: 22728824)
Am J Physiol Endocrinol Metab. 2004 Dec;287(6):E1154-65. (PMID: 15315905)
Proc Natl Acad Sci U S A. 2004 Jan 27;101(4):1087-92. (PMID: 14732702)
J Physiol. 2001 Aug 15;535(Pt 1):133-43. (PMID: 11507164)
Channels (Austin). 2011 Sep-Oct;5(5):402-9. (PMID: 21829087)
Proc Natl Acad Sci U S A. 2005 Mar 22;102(12):4643-8. (PMID: 15767570)
Annu Rev Physiol. 1988;50:409-26. (PMID: 3288099)
Nature. 2013 Jun 13;498(7453):190-7. (PMID: 23739333)
معلومات مُعتمدة: R56 DK047875 United States DK NIDDK NIH HHS
فهرسة مساهمة: Keywords: ACTH; KCNJ5; TREK-1; angiotensin II; human adrenal glomerulosa
المشرفين على المادة: 0 (G Protein-Coupled Inwardly-Rectifying Potassium Channels)
0 (KCNA4 protein, human)
0 (KCNJ5 protein, human)
0 (Kv1.4 Potassium Channel)
0 (Nerve Tissue Proteins)
0 (Potassium Channels, Tandem Pore Domain)
0 (potassium channel protein TREK-1)
11128-99-7 (Angiotensin II)
1F7A44V6OU (Colforsin)
1HQ3YCN4GS (potassium channel subfamily K member 3)
27YG812J1I (Arachidonic Acid)
4964P6T9RB (Aldosterone)
9002-60-2 (Adrenocorticotropic Hormone)
تواريخ الأحداث: Date Created: 20210526 Date Completed: 20210909 Latest Revision: 20220716
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC8321792
DOI: 10.1152/ajpcell.00118.2021
PMID: 34038243
قاعدة البيانات: MEDLINE
الوصف
تدمد:1522-1563
DOI:10.1152/ajpcell.00118.2021