Vascular-adrenal niche - Endothelial cell-mediated sensitization of human adrenocortical cells to angiotensin II

被引:20
作者
Ansurudeen, I.
Kopprasch, S.
Ehrhart-Bornstein, M.
Willenberg, H. S.
Krug, A. W.
Funk, R. H. W.
Bornstein, S. R.
机构
[1] Univ Technol Dresden, Carl Gustav Carus Med Sch, Med Clin 3, D-01307 Dresden, Germany
[2] Univ Technol Dresden, Carl Gustav Carus Med Sch, Inst Anat, D-01307 Dresden, Germany
[3] Univ Dusseldorf, Clin Endocrinol Diabetol & Rheumatol, D-4000 Dusseldorf, Germany
关键词
aldosterone; angiotensin II; forskolin; enclothelial cells; hyperaldosteronism;
D O I
10.1055/s-2006-948136
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Alterations in both vasculature and renin-angiotensin-aldosterone system are a consistent finding in the metabolic syndrome. Adrenal tissue is highly vascularized and encounters blood flow, exceeding by far the volume expected for its size. Endothelial cells in the adrenal vasculature are therefore a major cellular component of adrenocortical tissue. The aim of the study was to analyze the cellular interaction between endothelial and steroid producing cells, focusing on endothelial cell-factor-mediated activation of aldosterone synthesis. The interaction between human endothelial (HUVECs) cell-conditioned medium and human adrenocortical (NCI-H295R) cells in vitro induced a significant surge in aldosterone secretion. The endothelial cell-conditioned medium together with angiotensin 11 and forskolin also potentiated aldosterone release by 1.5-fold and 2.6-fold, respectively, while preincubation of NCI-H295R cells for 24h with endothelial cell-conditioned medium enhanced and sensitized the response of NCI-H295R to subsequent angiotensin 11 and forskolin stimuli by 2.5-fold and 2.2-fold, respectively. The increase in aldosterone release after preincubation with endothelial cell-conditioned medium was sensitive to cycloheximide and KN-93. Cellular conditioning with endothelial-cell factors exerts a hitherto unknown paracrine regulation of aldosterone production in human adrenocortical cells. This interaction may contribute to altered basal aldosterone release and have a role in patients with hypertension.
引用
收藏
页码:476 / 480
页数:5
相关论文
共 25 条
  • [1] Hypersensitivity of the adrenal cortex to trophic and secretory effects of angiotensin II in Lyon genetically-hypertensive rats
    Aguilar, F
    Lo, M
    Claustrat, B
    Saez, JM
    Sassard, J
    Li, JY
    [J]. HYPERTENSION, 2004, 43 (01) : 87 - 93
  • [2] Demonstration of an angiotensin II-induced negative feedback effect on aldosterone synthesis in isolated rat adrenal zona glomerulosa cells
    Aptel, HB
    Johnson, EIM
    Vallotton, MB
    Rossier, MF
    Capponi, AM
    [J]. MOLECULAR AND CELLULAR ENDOCRINOLOGY, 1996, 119 (01) : 105 - 111
  • [3] Bassett JR, 1997, MICROSC RES TECHNIQ, V36, P546, DOI 10.1002/(SICI)1097-0029(19970315)36:6<546::AID-JEMT11>3.0.CO
  • [4] 2-O
  • [5] Calmodulin-dependent kinase I regulates adrenal cell expression of aldosterone synthase
    Condon, JC
    Pezzi, V
    Drummond, BM
    Yin, S
    Rainey, WE
    [J]. ENDOCRINOLOGY, 2002, 143 (09) : 3651 - 3657
  • [6] The new biology of aldosterone
    Connell, JMC
    Davies, E
    [J]. JOURNAL OF ENDOCRINOLOGY, 2005, 186 (01) : 1 - 20
  • [7] Is altered adrenal steroid biosynthesis a key intermediate phenotype in hypertension?
    Connell, JMC
    Fraser, R
    MacKenzie, S
    Davies, E
    [J]. HYPERTENSION, 2003, 41 (05) : 993 - 999
  • [8] HUMAN ADRENAL GLAND WITH SPECIAL REFERENCE TO VASCULATURE
    DOBBIE, JW
    SYMINGTON, T
    [J]. JOURNAL OF ENDOCRINOLOGY, 1966, 34 (04) : 479 - +
  • [9] Intraadrenal interactions in the regulation of adrenocortical steroidogenesis
    Ehrhart-Bornstein, M
    Hinson, JP
    Bornstein, SR
    Scherbaum, WA
    Vinson, GP
    [J]. ENDOCRINE REVIEWS, 1998, 19 (02) : 101 - 143
  • [10] Human adipocytes secrete mineralocorticoid-releasing factors
    Ehrhart-Bornstein, M
    Lamounier-Zepter, V
    Schraven, A
    Langenbach, J
    Willenberg, HS
    Barthel, A
    Hauner, H
    McCann, SM
    Scherbaum, WA
    Bornstein, SR
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (24) : 14211 - 14216