scholarly journals NADPH Oxidase-Derived H2O2 Contributes to Angiotensin II-Induced Aldosterone Synthesis in Human and Rat Adrenal Cortical Cells

2012 ◽  
Vol 17 (3) ◽  
pp. 445-459 ◽  
Author(s):  
Senthilkumar B. Rajamohan ◽  
Gayatri Raghuraman ◽  
Nanduri R. Prabhakar ◽  
Ganesh K. Kumar
Keyword(s):  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Cortical Cells ◽  
Adrenal Cortical Cells

D4 dopamine receptor enhances angiotensin II-stimulated aldosterone secretion through PKC-ε and calcium signaling

2008 ◽  
Vol 294 (3) ◽  
pp. E622-E629 ◽  
Author(s):  
Hong-Wei Chang ◽  
Vin-Cent Wu ◽  
Chao-Yuan Huang ◽  
Hong-Yu Huang ◽  
Yung-Ming Chen ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mrna Level ◽  
Inhibitory Effect ◽  
Aldosterone Secretion ◽  
Inhibitory Peptide ◽  
Cortical Cells ◽  
Calcium Dependent ◽  
H295r Cells ◽  
Dopaminergic Regulation ◽  
Adrenal Cortical Cells

Aldosterone secretion is subjected to dopaminergic regulation. Our previous study showed that both human D2 and D4 dopamine receptors (D2R and D4R) modulate aldosterone secretion, but in opposing directions. The inhibitory effect of D2R is mediated by attenuating protein kinase C-μ (PKC-μ) and calcium-dependent signaling. The mechanism of D4R effect on angiotensin II (AII)-stimulated aldosterone secretion is explored in this study. Experiments were done with primary human adrenal cortical cells and human adrenocarcinoma (NCI-H295R) cells. Activation of different PKC isoforms was detected by specific phospho-PKC antibodies and PKC translocation. The role of calcium-dependent signaling was examined by measuring the cytoplasmic inositol 1,4,5-triphosphate (IP3) and calcium ([Ca2+]i). The D4R agonist PD-168,077 enhanced AII-stimulated aldosterone synthesis and secretion as early as 30 min following exposure independently of the modulation of aldosterone synthase (CYP11B2) transcription. CYP11B2 mRNA level elevated by AII was augmented by D4R in the later period. These effects were reversed by the D4R antagonist L-745,870. AII activated PKC-α/βII, -ε, and -μ but not PKC-δ, -θ, or -ζ/λ of H295R cells. The D4R agonist selectively enhanced AII-stimulated PKC-ε phosphorylation and its translocation to the cell membrane. Furthermore, the D4R agonist enhanced the AII-stimulated elevation of intracellular IP3 and [Ca2+]i. Inhibition of PKC-ε translocation by the PKC-ε-specific inhibitory peptide attenuated AII-stimulated aldosterone secretion, CYP11B2 mRNA expression, and elevation of intracellular IP3 and [Ca2+]i. We conclude that D4R augmented aldosterone synthesis/secretion induced by AII. The mechanisms responsible for this augmentation are mediated through enhancing PKC-ε phosphorylation and [Ca2+]i elevation.

Ultrastructural Cytopiasmic Changes of Adrenal Cortex During Pregnancy

1969 ◽  
Vol 27 ◽  
pp. 298-299
Author(s):  
T. M. Murad ◽  
Karen Israel ◽  
Jack C. Geer
Keyword(s):  
Adrenal Gland ◽  
Steroid Hormones ◽  
Adrenal Cortex ◽  
Lipid Droplets ◽  
Plasma Cholesterol ◽  
Adrenal Steroids ◽  
Dynamic Changes ◽  
Cortical Cells ◽  
Acetyl Coenzyme A ◽  
Adrenal Cortical Cells

Adrenal steroids are normally synthesized from acetyl coenzyme A via cholesterol. Cholesterol is also shown to enter the adrenal gland and to be localized in the lipid droplets of the adrenal cortical cells. Both pregnenolone and progesterone act as intermediates in the conversion of cholesterol into steroid hormones. During pregnancy an increased level of plasma cholesterol is known to be associated with an increase of the adrenal corticoid and progesterone. The present study is designed to demonstrate whether the adrenal cortical cells show any dynamic changes during pregnancy.

"STEROID-CELL" ANTIBODY IN ENDOCRINE DISEASES

1974 ◽  
Vol 76 (4) ◽  
pp. 729-740 ◽  
Author(s):  
Peter Kamp ◽  
Per Platz ◽  
Jørn Nerup
Keyword(s):  
Leydig Cells ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Hormone Production ◽  
Cortical Cells ◽  
Endocrine Diseases ◽  
Cell Antibody ◽  
Indirect Immunofluorescence Technique ◽  
Males And Females ◽  
Adrenal Cortical Cells

ABSTRACT By means of an indirect immunofluorescence technique, sera from 116 patients with Addison's disease, an equal number of age and sex matched controls and 97 patients with other endocrine diseases were examined for the occurrence of antibody to steroid-producing cells in ovary, testis and adrenal cortex. Fluorescent staining was observed in the theca cells of growing follicles, the theca lutein cells, testicular Leydig cells and adrenal cortical cells, i. e. cells which contain enzyme systems used in steroid hormone production. The "steroid-cell" antibody was present in 24 % of the patients with idiopathic Addison's disease, equally frequent in males and females, and in 17 % of the patients with tuberculous Addison's disease, but was rarely found in controls, including patients with other endocrine diseases. Female hypergonadotrophic hypogonadism made an exception, since the "steroid-cell" antibody was found in about half the cases with this condition.

Reactive Oxygen Species-Mediated Homologous Downregulation of Angiotensin II Type 1 Receptor Mrna by Angiotensin II

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 688-688
Author(s):  
Toshihiro Ichiki ◽  
Kotaro Takeda ◽  
Akira Takeshita
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Mrna Expression ◽  
Crucial Role ◽  
Oxygen Species ◽  
Ang Ii ◽  
Stimulation Of

58 Recent studies suggest a crucial role of reactive oxygen species (ROS) for the signaling of Angiotensin II (Ang II) through type 1 Ang II receptor (AT1-R). However, the role of ROS in the regulation of AT1-R expression has not been explored. In this study, we examined the effect of an antioxidant on the homologous downregulation of AT1-R by Ang II. Ang II (10 -6 mol/L) decreased AT1-R mRNA with a peak suppression at 6 hours of stimulation in rat aortic vascular smooth muscle cells (VSMC). Ang II dose-dependently (10 -8 -10 -6 ) suppressed AT1-R mRNA at 6 hours of stimulation. Preincubation of VSMC with N-acetylcysteine (NAC), a potent antioxidant, almost completely inhibited the Ang II-induced downregulation of AT1-R mRNA. The effect of NAC was due to stabilization of the AT1-R mRNA that was destabilized by Ang II. Ang II did not affect the promoter activity of AT1-R gene. Diphenylene iodonium (DPI), an inhibitor of NADH/NADPH oxidase failed to inhibit the Ang II-induced AT1-R mRNA downregulation. The Ang II-induced AT1-R mRNA downregulation was also blocked by PD98059, an extracellular signal-regulated protein kinase (ERK) kinase inhibitor. Ang II-induced ERK activation was inhibited by NAC as well as PD98059 whereas DPI did not inhibit it. To confirm the role of ROS in the regulation of AT1-R mRNA expression, VSMC were stimulated with H 2 O 2 . H 2 O 2 suppressed the AT1-R mRNA expression and activated ERK. These results suggest that production of ROS and activation of ERK are critical for downregulation of AT1-R mRNA. The differential effect of NAC and DPI on the downregulation of AT1-R mRNA may suggest the presence of other sources than NADH/NADPH oxidase pathway for ROS in Ang II signaling. Generation of ROS through stimulation of AT1-R not only mediates signaling of Ang II but may play a crucial role in the adaptation process of AT1-R to the sustained stimulation of Ang II.

scholarly journals Localization of a constitutively active, phagocyte-like NADPH oxidase in rabbit aortic adventitia: Enhancement by angiotensin II

1997 ◽  
Vol 94 (26) ◽  
pp. 14483-14488 ◽  
Author(s):  
P. J. Pagano ◽  
J. K. Clark ◽  
M. E. Cifuentes-Pagano ◽  
S. M. Clark ◽  
G. M. Callis ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Constitutively Active
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