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Aldosterone Release

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William B Campbell – 1st expert on this subject based on the ideXlab platform

  • angiotensin ii regulates adrenal vascular tone through zona glomerulosa cell derived eets and dhets
    Hypertension, 2011
    Co-Authors: Phillip G Kopf, Kathryn M Gauthier, David X Zhang, John R Falck, William B Campbell

    Abstract:

    Elevated concentrations of Aldosterone are associated with several cardiovascular diseases. Angiotensin II (Ang II) increases Aldosterone secretion and adrenal blood flow. This concurrent increase in steroidogenesis and adrenal blood flow is not understood. We investigated the role of zona glomerulosa (ZG) cells in the regulation of vascular tone of bovine adrenal cortical arteries by Ang II. ZG cells enhanced endothelium-dependent relaxations to Ang II. The ZG cell–dependent relaxations to Ang II were unchanged by removing the endothelium-dependent response to Ang II. These ZG cell–mediated relaxations were ablated by cytochrome P450 inhibition, epoxyeicosatrienoic acid (EET) antagonism, and potassium channel blockade. Analysis of ZG cell EET production by liquid chromatography/mass spectrometry demonstrated an increase in EETs and dihydroxyeicosatrienoic acids with Ang II stimulation. These EETs and dihydroxyeicosatrienoic acids produced similar concentration-dependent relaxations of adrenal arteries, which were attenuated by EET antagonism. Whole-cell potassium currents of adrenal artery smooth muscle cells were increased by Ang II stimulation in the presence of ZG cells but decreased in the absence of ZG cells. This increase in potassium current was abolished by iberiotoxin. Similarly, 14,15-EET induced concentration-dependent increases in potassium current, which was abolished by iberiotoxin. ZG cell Aldosterone Release was not directly altered by EETs. These data suggest that Ang II stimulates ZG cells to Release EETs and dihydroxyeicosatrienoic acids, resulting in potassium channel activation and relaxation of adrenal arteries. This provides a mechanism by which Ang II concurrently increases adrenal blood flow and steroidogenesis.

  • endothelium derived steroidogenic factor enhances angiotensin ii stimulated Aldosterone Release by bovine zona glomerulosa cells
    Endocrinology, 2007
    Co-Authors: Craig J Hanke, Blythe B Holmes, Yafei Xu, Kasem Nithipatikom, William B Campbell

    Abstract:

    Endothelium-derived steroidogenic factor (EDSF) is an endothelial peptide that stimulates Aldosterone Release from bovine adrenal zona glomerulosa (ZG) cells. The regulation of Aldosterone Release by combinations of EDSF and angiotensin II (AII) or EDSF and ACTH was investigated. Endothelial cells (ECs) and EC-conditioned media (ECCM) increased Aldosterone Release from ZG cells, an activity attributed to EDSF. AII (10−12 to 10−8 m) and ACTH (10−12 to 10−9 m) also stimulated the Release of Aldosterone from ZG cells. The stimulation by AII, but not ACTH, was greatly enhanced when ZG cells were coincubated with ECs. AII was metabolized by ECs to peptides identified by mass spectrometry as angiotensin (1-7) and angiotensin IV. There was very little metabolism of AII by ZG cells. Neither of these two AII metabolites altered Aldosterone Release from ZG cells, so they could not account for the enhanced response with ECs. AII-induced Aldosterone Release from ZG cells was enhanced by ECCM but not cell-free conditi…

  • adrenal capillary endothelial cells stimulate Aldosterone Release through a protein that is distinct from endothelin
    Endocrinology, 1999
    Co-Authors: Lori J Rosolowsky, William B Campbell, Craig J Hanke

    Abstract:

    We tested the possibility that bovine adrenal capillary endothelial cells (ECs) stimulate Aldosterone secretion from bovine zona glomerulosa (ZG) cells by the Release of a transferable factor. In coincubations of ZG cells and ECs in serum-free medium, Aldosterone Release was stimulated approximately 17-fold, and the stimulation was related to the concentration of ECs. The maximal stimulation by ECs was 75% of the maximal response to ACTH. In contrast, adrenal pericytes and fibroblasts were without effect. ECs incubated alone without ZG cells did not produce Aldosterone. Conditioned medium from ECs (EC-CM), but not adrenal fibroblasts, stimulated Aldosterone Release approximately 3-fold. The stimulation increased with the concentration of EC-CM and the duration of conditioning time. Steroidogenic activity in EC-CM was abolished by pronase treatment, indicating that the active factor was a protein. However, the activity in EC-CM was distinct from that of endothelin-1 (ET-1), an endothelial peptide that also…

Paulus S Wang – 2nd expert on this subject based on the ideXlab platform

  • effects of acrolein on Aldosterone Release from zona glomerulosa cells in male rats
    Steroids, 2016
    Co-Authors: Kailee Wang, Wenching Huang, Jouchun Chou, Tingchun Weng, Sindy Hu, Fukong Lieu, Galina Idova, Paulus S Wang

    Abstract:

    Abstract A positive correlation between smoking and hypertension has been well established. Acrolein is a major toxic volatile compound found in cigarette smoke. Human exposure to low levels of acrolein is unavoidable due to its production in daily activities, such as smoke from industrial, hot oil cooking vapors, and exhaust fumes from vehicles. The toxicity and the action mechanism of acrolein to induce apoptosis have been extensively studied, but the effects of acrolein on hypertension are still unknown. The present study aimed to examine the effects of acrolein on Aldosterone Release both in vivo and in vitro. Male rats were divided into three groups, and intraperitoneally injected with normal saline, or acrolein (2 mg/kg) for 1 (group A-1) or 3 (group A-3) days, respectively. After sacrificing, rat blood samples were obtained to measure plasma Aldosterone and angiotensin II (Ang II) levels. Zona glomerulosa (ZG) cells were prepared from rat adrenal cortex, and were incubated with or without stimulants. We found that the serum Aldosterone was increased by 1.2-fold (p

  • effects of propylthiouracil on the production of Aldosterone in rat zona glomerulosa cells
    Adaptive Medicine, 2012
    Co-Authors: Hsiaofung Pu, Paulus S Wang

    Abstract:

    Propylthiouracil (PTU), an anti-thyroid drug, is widely used for the treatment in hyperthyroid patients. Previous studies indicate that thyroxine inhibit the spontaneous and adrenocorticotropin (ACTH)-stimulated corticosterone secretion by acting directly at adrenal glands via decrease cAMP production. It has also been shown that PTU suppresses corticosterone Release by male rat zona fasciculata-reticularis cells. However, the direct effects and mechanisms of PTU on the Aldosterone production in adrenal zona glomerulosa (ZG) cells are still unclear. ZG cells were prepared from adrenocortical tissues of male rats, and then challenged with or without angiotensin II (10^(-7), 10^(-6) M), ACTH (10^(-9) M), A23187 (10^(-5) M), cyclopiazonic acid (CPA, 10^(-5) M), forskolin (10^(-5) M), 8-Br-cAMP (10^(-5) M), trilostane (10^(-6) M, 3β-HSD inhibitor) or steroidogenic precursors (e.g. 10^(-6) M 25-OH-cholesterol and 10^(-7), 10^(-5) M corticosterone) at 37°C for 1 h. Our results showed that PTU (0-3 mM) dose-dependently decreased the Aldosterone Release in response to the above hormones, drugs and the steroidogenic precursors in vitro. PTU also decreased steroidogenic acute regulatory (StAR) protein expression, but did not alter the protein expression of P450 side chain cleavage enzyme (P450scc) during steroidogenesis of Aldosterone. These results suggested that PTU has a direct inhibitory effect on Aldosterone production via cAMP, and Ca^2+ down stream pathway and the steroidogenic enzymes activities including P450scc and Aldosterone synthase, as well as StAR protein expression.

  • effects of nonylphenol on Aldosterone Release from rat zona glomerulosa cells
    Chemico-Biological Interactions, 2012
    Co-Authors: Lingling Chang, Paulus S Wang

    Abstract:

    Abstract Alkylphenol ethoxylate, which consists of approximately 80% nonylphenol ethoxylate (NPE), is a major nonionic surfactant. Nonylphenol (NP), the primary degradation product of NPE, has been reported to interfere with reproduction in fish, reptiles, and mammals by inducing cell death in the gonads and by affecting other reproductive parameters. However, the effects of NP on rat adrenal zona glomerulosa cells (ZG) and the underlying mechanisms remain unclear. In this study, we explored the effects of NP on Aldosterone Release. ZG cells were incubated with NP in the presence or absence of the secretagogues angiotensin II (ANG II), potassium, 8-Br-cAMP, 25-OH-cholesterol, corticosterone or cyclopiazonic acid (CPA). After performing radioimmunoassay (RIA) and Western blot analysis, we found that (1) NP stimulated Aldosterone Release in cells induced by ANG II, KCl, 8-Br-cAMP, 25-OH-cholesterol, corticosterone, and CPA; (2) NP triggered the Release of higher amounts of pregnenolone in cells treated with vehicle and 25-OH-cholesterol + trilostane than in cells treated with other compounds; and (3) the stimulatory effect of NP seemed to be mediated through steroidogenic acute regulatory protein (StAR) and Aldosterone synthase activity. These observations suggest that the effects of NP are mediated via increased free Ca2+ in the cytoplasm.

Craig J Hanke – 3rd expert on this subject based on the ideXlab platform

  • endothelium derived steroidogenic factor enhances angiotensin ii stimulated Aldosterone Release by bovine zona glomerulosa cells
    Endocrinology, 2007
    Co-Authors: Craig J Hanke, Blythe B Holmes, Yafei Xu, Kasem Nithipatikom, William B Campbell

    Abstract:

    Endothelium-derived steroidogenic factor (EDSF) is an endothelial peptide that stimulates Aldosterone Release from bovine adrenal zona glomerulosa (ZG) cells. The regulation of Aldosterone Release by combinations of EDSF and angiotensin II (AII) or EDSF and ACTH was investigated. Endothelial cells (ECs) and EC-conditioned media (ECCM) increased Aldosterone Release from ZG cells, an activity attributed to EDSF. AII (10−12 to 10−8 m) and ACTH (10−12 to 10−9 m) also stimulated the Release of Aldosterone from ZG cells. The stimulation by AII, but not ACTH, was greatly enhanced when ZG cells were coincubated with ECs. AII was metabolized by ECs to peptides identified by mass spectrometry as angiotensin (1-7) and angiotensin IV. There was very little metabolism of AII by ZG cells. Neither of these two AII metabolites altered Aldosterone Release from ZG cells, so they could not account for the enhanced response with ECs. AII-induced Aldosterone Release from ZG cells was enhanced by ECCM but not cell-free conditi…

  • adrenal capillary endothelial cells stimulate Aldosterone Release through a protein that is distinct from endothelin
    Endocrinology, 1999
    Co-Authors: Lori J Rosolowsky, William B Campbell, Craig J Hanke

    Abstract:

    We tested the possibility that bovine adrenal capillary endothelial cells (ECs) stimulate Aldosterone secretion from bovine zona glomerulosa (ZG) cells by the Release of a transferable factor. In coincubations of ZG cells and ECs in serum-free medium, Aldosterone Release was stimulated approximately 17-fold, and the stimulation was related to the concentration of ECs. The maximal stimulation by ECs was 75% of the maximal response to ACTH. In contrast, adrenal pericytes and fibroblasts were without effect. ECs incubated alone without ZG cells did not produce Aldosterone. Conditioned medium from ECs (EC-CM), but not adrenal fibroblasts, stimulated Aldosterone Release approximately 3-fold. The stimulation increased with the concentration of EC-CM and the duration of conditioning time. Steroidogenic activity in EC-CM was abolished by pronase treatment, indicating that the active factor was a protein. However, the activity in EC-CM was distinct from that of endothelin-1 (ET-1), an endothelial peptide that also…

  • prostaglandin e2 induced Aldosterone Release is mediated by an ep2 receptor
    Hypertension, 1998
    Co-Authors: Stephen Csukas, Craig J Hanke, David Rewolinski, William B Campbell

    Abstract:

    Abstract —Prostaglandin E2 (PGE2) is an endogenous hormone of adrenal zona glomerulosa cells and is Released in response to stimulation by agonists such as angiotensin II (Ang II). It stimulates the Release of Aldosterone from cultured bovine adrenal zona glomerulosa cells. These studies were designed to determine whether this steroidogenic effect of PGE2 was mediated by an EP1, EP2, or EP3 receptor. Prostaglandin E2 and 11-deoxy PGE1, an EP2-selective agonist, stimulated Aldosterone Release in a concentration-related manner with an ED50 of 300 nmol/L for PGE2 and 2 μmol/L for 11-deoxy PGE1. The maximal effect of PGE2 was less than that of angiotensin II. 17-Phenyl trinor PGE2, an EP1-selective agonist, required concentrations of 100 μmol/L to stimulate Aldosterone Release and sulprostone, an EP3/EP1-selective agonist, failed to alter Aldosterone Release. The EP1-selective antagonist SC19220 failed to alter basal or PGE2-stimulated Aldosterone Release over a range of concentrations. PGE2 and 11-deoxy PGE1 also stimulated an increase in both intracellular and extracellular cAMP. This increase was time- and concentration-related. The ED50 for PGE2 was 9.8 μmol/L. 17-Phenyl trinor PGE2 and sulprostone were without effect. Using fura-2 loaded cells, PGE2 (2 μmol/L), dibutyryl cAMP (2 mmol/L), and Ang II (2 μmol/L) increased intracellular calcium over basal concentrations by 5.5-fold, 3-fold, and 6.2-fold, respectively. Like PGE2, dibutyryl cAMP also stimulated Aldosterone Release. PGE2- and dibutyryl cAMP–induced Aldosterone Release were blocked by the calcium channel inhibitor diltiazem. These studies indicate that PGE2 is a potent stimulus for Aldosterone Release and that the effect is mediated by EP2 receptors. Both cAMP and calcium appear to mediate the steroidogenic effect of PGE2 and calcium seems to be distal to cAMP.