Aldosterone Release

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William B Campbell - One of the best experts 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: William B Campbell, Lori J Rosolowsky, 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.

  • 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.

Paulus S Wang - One of the best experts 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.

  • effects of dehydroepiandrosterone on Aldosterone Release in rat zona glomerulosa cells
    Journal of Biomedical Science, 2008
    Co-Authors: Lingling Chang, Paulus S Wang
    Abstract:

    The present study was to investigate the effects and action mechanisms of dehydroepiandrosterone (DHEA) on steroidogenesis in rat adrenal zona glomerulosa cells (ZG). ZG cells were incubated with DHEA in the presence or absence of angiotensin II (AngII), a high concentration of potassium, 8-Br-cAMP, forskolin, 25-OH-cholesterol, pregnenolone, progesterone, deoxycorticosterone, corticosterone, A23187, or cyclopiazonic acid (CPA) at 37°C for 1 h. The concentration of Aldosterone or pregnenolone in the culture medium was then measured by radioimmunoassay (RIA). The cells were used to determine the cellular cAMP content. The data demonstrated that: (1) DHEA inhibited AngII-, high concentration of KCl-, forskolin-, 8-Br-cAMP-, 25-OH-cholesterol-, pregnenolone-, progesterone-, deoxycorticosterone-, corticosterone-, A23187-, or CPA-stimulated Aldosterone Release; (2) DHEA increased 25-OH-cholesterol-stimulated pregnenolone Release but not when 25-OH-cholesterol was combined with trilostane; (3) DHEA noncompetitively inhibited Aldosterone synthase but showed uncompetitive inhibition of P450scc. These results suggest that DHEA acts directly on rat ZG cells to diminish Aldosterone secretion by inhibition of a post-cAMP pathway or by acting on intracellular Ca2+ mobilization. In addition it affects the function of post-P450scc steroidogenic enzymes.

  • inhibitory effect of evodiamine on Aldosterone Release by zona glomerulosa cells in male rats
    Chinese Journal of Physiology, 2001
    Co-Authors: Peihsuan Hung, Geuijane Wang, Chiehfu Chen, Paulus S Wang
    Abstract:

    : Evodiamine is a bioactive alkaloid extracted from a Chinese herb named Wu-Chu-Yu, which possesses thermoregulatory, analgesic, and cardiovascular effects. Some studies have demonstrated that evodiamine reduces blood pressure through acting on endothelium and smooth muscle cells to produce a vasodilatory effect, but whether it affects Aldosterone secretion is unclear. The purpose of this study was to examine the effect of evodiamine on Aldosterone Release in adrenal zona glomerulosa (ZG) cells. ZG cells were isolated from the adrenal glands of adult male rats and incubated with angiotensin II (Ang II, 1x10(-7) M) and 3H-pregnenolone in the presence or absence of evodiamine (1x10(-6)-1x10(-3) M) at 37 degrees C for one hour. The concentration of Aldosterone in the media was measured by a radioimmunoassay. The level of radioactivity incorporated into Aldosterone and its precursors after incubation of ZG cells with 3H-pregnenolone was analyzed by thin-layer chromatography. The results demonstrated that evodiamine decreased the basal level of and Ang II-induced Release level of Aldosterone in rat ZG cells. Administration of evodiamine also decreased the level of radioactivity incorporated into 3H-corticosterone and 3H-Aldosterone following incubation of ZG cells with 3H-pregnenolone. This suggest that evodiamine affects Aldosterone Release in rat adrenal glomerulosa cells by acting on Ang II-associated pathway and reducing the activity of 11 beta-hydroxylase (an enzyme which coverts deoxycorticosterone to corticosterone) during the steroidogenesis of Aldosterone.

Craig J Hanke - One of the best experts 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: William B Campbell, Lori J Rosolowsky, 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.

  • 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.

Hershel Raff - One of the best experts on this subject based on the ideXlab platform.

  • Aldosterone Release from adrenal cells is inhibited by reduced oxygen levels in vitro during maturation in rabbits
    Reproduction Fertility and Development, 1996
    Co-Authors: Paula E Papanek, Barbara M. Jankowski, Hershel Raff
    Abstract:

    Hypoxia in vivo leads to a decrease in Aldosterone not completely explained by extrinsic controllers of adrenal function including adrenocorticotrophic hormone, renin-angiotensin II, and K+. The dissociation of renin and Aldosterone during acute hypoxia in vivo may be explained by the finding that Aldosterone synthesis in adrenal cells is reversibly and specifically inhibited by decreases in O2 levels within the physiological range. The present study investigated whether the direct effect of acute decreases in O2 levels on aldosteronogenic pathway is altered during maturation. Adrenal cells (whole adrenals) were prepared from fetal (27 days gestation), neonatal (1 day), and infant (10 days) New Zealand White rabbits, and capsular cells were prepared from young (21 days) and adult (3 months) rabbits. All cells were dispersed with collagenase. Basal and cAMP-stimulated Aldosterone production were assessed under two different levels of O2 (pO2 = 20.0 kPa or pO2 = 8.7 kPa). Decreased O2 levels significantly inhibited cAMP-stimulated Aldosterone production in cells obtained from rabbits of all ages by 60 +/- 5% cAMP-stimulated Aldosterone production was significantly lower in cells obtained from neonates and premature animals under both normoxic and reduced O2 conditions as compared with animals > or = 10 days old. Corticosterone production by cells obtained from adults and 21-day-old rabbits was unaffected by reduced O2 conditions suggesting a specific effect on the Aldosterone pathway. The data demonstrate that the O2 sensitivity of the Aldosterone pathway is present throughout development.

  • inhibition of Aldosterone Release by hypoxia in vitro interaction with carbon monoxide
    Journal of Applied Physiology, 1994
    Co-Authors: Hershel Raff, Barbara M. Jankowski
    Abstract:

    We have demonstrated that the aldosteronogenic pathway of the zona glomerulosa is unusually sensitive to modest changes in PO2 (Michaelis constant for O2 approximately 95 Torr). The current study evaluated the interaction of CO (the classic ligand for P-450 enzymes) and the decreases in O2 on aldosteronogenesis in vitro. Bovine adrenocortical zona glomerulosa cells were incubated for 2 h and stimulated with either adenosine 3′,5′-cyclic monophosphate (cAMP) or angiotensin II. Ten and 20% CO led to significant decreases in cAMP- and angiotensin II-stimulated aldosteronogenesis. The combination of 20% CO and moderate decreases in PO2 (from approximately 140 to approximately 100 Torr) led to an interactive decrease in Aldosterone production. The conversion of corticosterone to Aldosterone catalyzed by Aldosterone synthase, which is the site of O2 sensitivity, was not significantly inhibited by CO. We conclude that the Aldosterone pathway is not exceptionally sensitive to CO compared with other steroidogenic pathways. This observation suggests that the unique O2-sensitive properties of the Aldosterone pathway located primarily within Aldosterone synthase may not reside in its CO binding site (i.e., heme).

  • Effect of CO2/pH on the Aldosterone response to hypoxia in bovine adrenal cells in vitro.
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 1993
    Co-Authors: Hershel Raff, Barbara M. Jankowski
    Abstract:

    Acidosis increases and hypoxia decreases Aldosterone production from the adrenal zona glomulerosa in vivo, in situ, and in vitro. These effects appear to be located at different steps in the steroidogenic process. Because respiratory acidosis and hypoxemia are common sequelae of chronic lung disease, the present experiments evaluated the interaction of hypoxia and CO2 (with uncompensated or compensated extracellular pH) on aldosteronogenesis in vitro. Bovine adrenal zona glomerulosa cells were stimulated with angiotensin II (ANG II) or adenosine 3',5'-cyclic monophosphate under room air control (21% O2-0% CO2), CO2 per se (21% O2-10% CO2), hypoxia per se (10% O2-0% CO2), and the combination of CO2 and hypoxia (10% O2-10% CO2). Furthermore, under CO2, pH was either allowed to decrease from 7.2 to 6.8 (uncompensated) or its decrease was minimized (> 7.05) with NaOH (compensated). CO2 without pH compensation led to a significant increase in ANG II-stimulated Aldosterone Release; when the decrease in pH was minimized, CO2 inhibited ANG II-stimulated Aldosterone Release. Hypoxia inhibited Aldosterone Release; the inhibitory effect of hypoxia predominated when combined with CO2. In the presence of cyanoketone, pregnenolone production from endogenous precursors (early pathway) was unaffected. However, the conversion of corticosterone to Aldosterone (late pathway) was inhibited by low O2 but unaffected by CO2. It is concluded that the inhibitory effect of low O2 on the late pathway predominates over the effects of uncompensated or compensated simulated respiratory acidosis on aldosteronogenesis.

  • oxygen sensitivity of potassium and angiotensin ii stimulated Aldosterone Release by bovine adrenal cells
    Journal of Endocrinology, 1991
    Co-Authors: Robert C Brickner, Hershel Raff
    Abstract:

    : Angiotensin II (AII) and extracellular K+, acting through different intracellular mechanisms, stimulate Aldosterone Release in a synergistic fashion. We have previously shown that decreases in oxygen (O2) within the physiological range inhibit AII, cyclic AMP (cAMP) and ACTH-stimulated Aldosterone Release. The present experiment evaluated the effect of various concentrations of O2 on K+-stimulated Aldosterone Release in the presence and absence of AII. Dispersed bovine adrenal glomerulosa cells were incubated with different concentrations of K+ (0.9-5.4 mmol/l) without and with AII (10 nmol/l) under different concentrations of O2 (0, 5 or 50%); 21% O2 (pO2 = 19.9 +/- 0.5 kPa,n = 9) was used as reference control for comparison. In all cases, increases in K+ stimulated Aldosterone Release, an effect augmented by AII. Under 0% O2 (pO2 = 8.1 +/- 0.3 kPa, n = 3) and 5% O2 (pO2 = 12.8 +/- 0.5 kPa, n = 3), Aldosterone Release stimulated by K+ or K+/AII was significantly inhibited compared with that under 21% O2. Conversely, under 50% O2 (pO2 = 36.3 +/- 2.5 kPa, n = 3), Aldosterone Release stimulated by K+ or K+/AII was significantly augmented. Cortisol secretion was not significantly affected by 5% or 50% O2 but was significantly decreased under 0% O2. The effect of O2 on K+/AII stimulation of Aldosterone Release, as well as previous experiments with cAMP, progesterone and ACTH, suggest a final common post-receptor oxygen-sensitive component of the Aldosterone synthetic pathway. It is suggested that one or more enzymes in the Aldosterone synthetic pathway is/are exquisitely sensitive to small changes in O2 within the physiological range.

  • the effect of oxygen on Aldosterone Release from bovine adrenocortical cells in vitro po2 versus steroidogenesis
    Endocrinology, 1990
    Co-Authors: Hershel Raff, Saeid Kohandarvish, Arbara Jankowski
    Abstract:

    Hypoxia decreases plasma Aldosterone in vivo without a decrease in PRA, angiotensin II (ANG II), ACTH, or cortisol. The present study evaluated whether this could be due to a direct, specific inhibitory effect on the zona glomerulosa related to the magnitude of the decrease in oxygen (O2). Bovine adrenocortical cells were dispersed with collagenase and studied in vitro within 48 h. Cells were stimulated for 2 h with ANG II (0.1-1000 nM) or (Bu)2cAMP (0.3-3 mM) under oxygen levels ranging from 0 to 100% O2 (PO2 from 66 ± 4 to 561 ± 46 torr) vs. a reference gas mixture (21% O2 PO2 -140 torr). Exposure to 123 ± 8, 110 ± 12, 100 ± 16, and 66 ± 4 torr led to 27%, 30%, 40% and 70% inhibition, respectively, of 3 nM ANG II-stimulated Aldosterone secretion as compared to 140 ± 16 torr (reference). Exposure to hyperoxia (288 ± 36 to 561 ± 46 torr) led to a small (10%) increase in ANG II-stimulated Aldosterone secretion which was not statistically significant. The P50 (half-maximal PO2) for aldosteronogenesis was ap...

Lori J Rosolowsky - One of the best experts on this subject based on the ideXlab platform.

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

  • endothelial cells stimulate Aldosterone Release from bovine adrenal zona glomerulosa cells
    American Journal of Physiology-endocrinology and Metabolism, 1994
    Co-Authors: Lori J Rosolowsky, William B Campbell
    Abstract:

    Intra-adrenal factors promote basal as well as adrenocorticotropic hormone (ACTH)-, angiotensin-, and flow-induced steroid secretion. Because endothelial cells respond to changes in flow and are in...

  • bradykinin stimulates Aldosterone Release from cultured bovine adrenocortical cells through bradykinin b2 receptors
    Endocrinology, 1992
    Co-Authors: Lori J Rosolowsky, William B Campbell
    Abstract:

    The adrenal cortex contains a kallikrein-like enzyme that may lead to bradykinin (BK) formation. This study was designed to determine whether BK acts on adrenocortical cells to stimulate steroid secretion. BK, Lys-BK, a specific BK 2 (B2) receptor agonist, and desArg9-BK, a specific BK 1 (B1) receptor agonist, all stimulated Aldosterone secretion from cultured bovine adrenal zona glomerulosa cells. BK and Lys-BK were equipotent (EC50 = 2 x 10(-9) M), whereas desArg9-BK was 1000-fold less potent. The maximal effects of BK and BK analogs were comparable to the maximal effects of adrenocorticotropin or angiotensin II. A B2, but not a B1, receptor antagonist inhibited BK-stimulated Aldosterone Release. Verapamil and N,N-diethylamino-octyl-3,4,5-trimethoxybenzoate, which reduce intracellular calcium concentrations, reduced BK-stimulated Aldosterone secretion. Although BK stimulated both prostacyclin and Aldosterone production, indomethacin abolished prostacyclin production without affecting Aldosterone secreti...

  • endothelin enhances adrenocorticotropin stimulated Aldosterone Release from cultured bovine adrenal cells
    Endocrinology, 1990
    Co-Authors: Lori J Rosolowsky, William B Campbell
    Abstract:

    Endothelin (ET) is an endothelial cell-derived peptide with profound hemodynamic effects. We investigated the effects of ET on steroid Release from bovine adrenal cortical cells. ET-1 (10-1110-6 M) did not alter basal Aldosterone Release from adrenal glomerulosa cells. However, both angiotensin-II (All)- and ACTH-stimulated Aldosterone Release from these cells. ET-1 enhanced ACTH-stimulated Aldosterone Release over a range of concentrations. This enhancement was observed at a threshold of 0.1 nM ET-1. Similar responses were observed in incubations of 1- and 2-h duration. In contrast, All-stimulated Aldosterone Release was not altered by ET-1. ET-1 also enhanced Aldosterone Release in cells stimulated with 8-bromo-cAMP. All increased cytoplasmic Ca2+ concentrations in fura-2-loaded cells; however, ET-1 alone or with ACTH had no effect. In addition, chronic treatment of cells with ACTH for 2 days caused an enhanced Release of Aldosterone in cells acutely treated with ET- 1 compared to cells not acutely trea...