Efflux of potassium ions in angiotensin II-stimulated bovine adrenocortical cells

1991 ◽  
Vol 128 (2) ◽  
pp. 297-304 ◽  
Author(s):  
R. M. Shepherd ◽  
R. Fraser ◽  
D. J. Nichols ◽  
C. J. Kenyon
Keyword(s):  
Angiotensin Ii ◽  
Cell Membrane ◽  
Slow Component ◽  
Electrical Potential ◽  
Potassium Ions ◽  
Adrenocortical Cell ◽  
Efflux Rate ◽  
Adrenocortical Cells ◽  
Fast Exchange ◽  
Stimulation Of

ABSTRACT Angiotensin II (AII) stimulation of steroidogenesis is known to be associated with depolarization of the adrenocortical cell membrane. In these cells, membrane permeability to potassium ions governs electrical potential. The effects of All on the rate of efflux of K+ in relation to the control of aldosterone synthesis has been investigated in bovine adrenocortical cells preloaded with 43K. In static incubations, the pattern of 43K efflux fitted a model with two exponential components with t½ values of 47·7±1·7 and 14·2±0·6 (s.e.m.) min. AII increased the efflux rate of the slow-exchange component (t½ 37·1±0·6 min) and retarded efflux from the fast-exchange component. With ouabain present to prevent reuptake of the isotope, the rate of efflux for both components was increased in unstimulated cells (t½ 28·4±1·1 and 12·0±0·7 min). AII again increased the rate of efflux from the slow component (t½ = 24·2±1·7 min, P < 0·01) and retarded efflux from the fast component. These biphasic effects were apparent in cells treated with a range of AII concentrations (0·1 nmol/l–1 μmol/l) but the point in time at which increased efflux from the slower component predominated over retardation of the slow component was earlier for cells treated with 1 μmol AII/l than for cells treated with lower concentrations. We suggest that decreases and increases in K+ efflux caused by AII are associated with depolarization and repolarization respectively. Changes in intracellular concentrations of Ca2+ may link these events. Journal of Endocrinology (1991) 128, 297–304

The Effect of External Potassium Ions on the Electrical Potential Measured Across the Gills of the Teleost, Dormitator Maculatus

1974 ◽  
Vol 61 (2) ◽  
pp. 277-283
Author(s):  
DAVID H. EVANS ◽  
JEFFREY C. CARRIER ◽  
MARGARET B. BOGAN
Keyword(s):  
Sea Water ◽  
Electrical Potential ◽  
Potassium Ions ◽  
Sodium Efflux ◽  
Electrical Potentials ◽  
External Potassium ◽  
Potassium Influx ◽  
Sodium Extrusion ◽  
Sufficient Magnitude ◽  
Stimulation Of

1. A technique has been developed for the measurement of electrical potentials (TGP's) across the gills of free-swimming, Dormitator maculatus. 2. Transfer of fish to various KCl solutions is correlated with changes in the TGP, which are not of sufficient magnitude to account for the known potassium stimulation of sodium efflux from this species. 3. Transfer to potassium-free sea water results in little or no change in TGP while previous results have shown that such a transfer is correlated with a 22% reduction of sodium efflux. 4. Transfer to fresh water results in a reduction of TGP from +17 mV (inside positive) to -36 mV which is sufficient to account for the instantaneous reduction in sodium efflux previously shown for this species. 5. It is concluded that while changes in TGP can account for the ‘Na-free effect’ in D. maculatus they cannot account for the potassium effects on sodium extrusion. This supports the previous conclusion that sodium efflux and potassium influx are chemically linked in this species.

Actions of desacetyl-α-melanocyte-stimulating hormone on human adrenocortical cells

1989 ◽  
Vol 121 (3) ◽  
pp. 579-583 ◽  
Author(s):  
K. L. Henville ◽  
J. P. Hinson ◽  
G. P. Vinson ◽  
S. M. Laird
Keyword(s):  
Angiotensin Ii ◽  
Physiological Role ◽  
Effective Concentration ◽  
Adrenocortical Function ◽  
Cortisol Secretion ◽  
Adrenocortical Cells ◽  
Minimum Effective Concentration ◽  
Maximal Stimulation ◽  
Significant Stimulation ◽  
Stimulation Of

ABSTRACT The responses of human adrenocortical cells to stimulation by ACTH(1–24), desacetyl-α-MSH, α-MSH and angiotensin II amide have been compared. Both desacetyl-α-MSH, thought to be the major form of the peptide in the human pituitary and in circulating plasma, and α-MSH caused a significant stimulation of aldosterone, corticosterone and cortisol secretion. Significant stimulation of the production of these steroids was obtained with desacetyl-α-MSH at a concentration of 1 nmol/l, while the response to α-MSH was considerably less sensitive, with a minimum effective concentration of 0·1 μmol/l. These values compared with minimum effective concentrations of 1 pmol/l for ACTH and 0·1 μmol/l for angiotensin II amide. Although cell types were not separated, it is possible to conclude that none of the peptides showed any specificity for the zona glomerulosa, and in each case the same minimum effective concentration of peptide was required for both aldosterone and cortisol secretion. Yields of steroid obtained under conditions of maximal stimulation by ACTH(1–24), α-MSH and desacetyl-α-MSH were at least three to five times the basal output of aldosterone, four to eight times that for corticosterone and more than seven to sixteen times that for cortisol. Angiotensin II amide was a relatively poor stimulant with maximal stimulation only 1·5 × basal. In these experiments the minimum effective concentration for desacetyl-α-MSH (1 nmol/l) was close to the circulating concentration of desacetyl-α-MSH (0·3 nmol/l) in man, and it is thus possible that this peptide may have a physiological role in the control of adrenocortical function. Journal of Endocrinology (1989) 121, 579–583

scholarly journals Angiotensin II-Induced Expression of Brain-Derived Neurotrophic Factor in Human and Rat Adrenocortical Cells

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1695-1703 ◽  
Author(s):  
Mária Szekeres ◽  
György L. Nádasy ◽  
Gábor Turu ◽  
Katinka Süpeki ◽  
László Szidonya ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Ang Ii ◽  
Bdnf Expression ◽  
Adrenocortical Cells ◽  
H295r Cells ◽  
Glomerulosa Cells ◽  
Stimulation Of

Angiotensin II (Ang II) is a major regulator of steroidogenesis in adrenocortical cells, and is also an effective inducer of cytokine and growth factor synthesis in several cell types. In microarray analysis of H295R human adrenocortical cells, the mRNA of brain-derived neurotrophic factor (BDNF), a neurotrophin widely expressed in the nervous system, was one of the most up-regulated genes by Ang II. The aim of the present study was the analysis of the Ang II-induced BDNF expression and BDNF-induced effects in adrenocortical cells. Real-time PCR studies have shown that BDNF is expressed in H295R and rat adrenal glomerulosa cells. In H295R cells, the kinetics of Ang II-induced BDNF expression was faster than that of aldosterone synthase (CYP11B2). Inhibition of calmodulin kinase by KN93 did not significantly affect the Ang II-induced stimulation of BDNF expression, suggesting that it occurs by a different mechanism from the CYP11B2-response. Ang II also caused candesartan-sensitive, type-1 Ang II receptor-mediated stimulation of BDNF gene expression in primary rat glomerulosa cells. In rat adrenal cortex, BDNF protein was localized to the subcapsular region. Ang II increased BDNF protein levels both in human and rat cells, and BDNF secretion of H295R cells. Ang II also increased type-1 Ang II receptor-mediated BDNF expression in vivo in furosemide-treated rats. In rat glomerulosa cells, BDNF induced tropomyosin-related kinase B receptor-mediated stimulation of EGR1 and TrkB expression. These data demonstrate that Ang II stimulates BDNF expression in human and rat adrenocortical cells, and BDNF may have a local regulatory function in adrenal glomerulosa cells.

scholarly journals Microribonucleic Acid-21 Increases Aldosterone Secretion and Proliferation in H295R Human Adrenocortical Cells

Endocrinology ◽  
2008 ◽  
Vol 149 (5) ◽  
pp. 2477-2483 ◽  
Author(s):  
Damian G. Romero ◽  
Maria W. Plonczynski ◽  
Cristian A. Carvajal ◽  
Elise P. Gomez-Sanchez ◽  
Celso E. Gomez-Sanchez
Keyword(s):  
Cell Proliferation ◽  
Angiotensin Ii ◽  
Cell Line ◽  
Biologically Active ◽  
Cell Physiology ◽  
Adrenocortical Cell ◽  
Aldosterone Secretion ◽  
Adrenocortical Cells ◽  
Expression Levels ◽  
H295r Cells

MicroRNAs (miRNAs) are endogenous small noncoding RNAs that decrease the expression levels of specific genes by translational repression, sequestration, and degradation of their mRNAs. Angiotensin II is an important modulator of adrenal zona glomerulosa cell physiology, including steroidogenesis and proliferation among many other physiological processes. Because each miRNA may regulate the expression levels of multiple genes, thereby resembling the transcription regulatory networks triggered by transcription factors, we hypothesize that specific miRNAs may be involved in angiotensin II-mediated adrenocortical cell physiology. The human adrenocortical cell line H295R is the only adrenal cell line available with a steroid secretion pattern and regulation similar to freshly isolated adrenocortical cells. We screened for miRNAs regulated by angiotensin II in H295R cells and found that miRNA-21 expression levels were specifically modulated by angiotensin II. Angiotensin II time dependently increased miRNA-21 expression reaching a 4.4-fold induction after 24 h. Angiotensin II-mediated miRNA-21 expression resulted in biologically active miRNA-21, determined using a fusion mRNA reporter system carrying miRNA-21 target sequences in its 3′ untranslated region. Up-regulation of miRNA-21 intracellular levels increased aldosterone secretion but not cortisol. Elevation of miRNA-21 levels also increased cell proliferation in H295R cells. In summary, miRNA-21 is an endogenously expressed miRNA in human adrenal cells. miRNA-21 expression is up-regulated by angiotensin II, and its overexpression caused an increase in aldosterone secretion and cell proliferation. Alterations in miRNA-21 expression levels or function may be involved in dysregulation of angiotensin II signaling and abnormal aldosterone secretion by adrenal glands in humans.

Activator protein-1 is necessary for angiotensin-II stimulation of human adrenocorticotropin receptor gene transcription

2001 ◽  
Vol 268 (6) ◽  
pp. 1802-1810
Author(s):  
Danielle Naville ◽  
Estelle Bordet ◽  
Marie-Claude Berthelon ◽  
Philippe Durand ◽  
Martine Begeot
Keyword(s):  
Angiotensin Ii ◽  
Gene Transcription ◽  
Receptor Gene ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
Stimulation Of

Use of Isolated Tight Epithelia to Study the Site and Mode of Drug Action on Cell Membrane Transport: Effect of the Antipsychotic Agent Trifluoperazine

1990 ◽  
Vol 17 (3) ◽  
pp. 224-227
Author(s):  
Henning F. Bjerregaard
Keyword(s):  
Cell Membrane ◽  
Toxic Effect ◽  
Membrane Transport ◽  
Antipsychotic Agent ◽  
Na Transport ◽  
Tight Epithelia ◽  
Acute Toxic Effect ◽  
Cell Membrane Transport ◽  
Dose Dependent ◽  
Stimulation Of

The aim of the present study was to investigate the site and mode of trifluoperazine (TFP) action on cell membrane transport by the use of isolated frog skin. This cellular system gives access to the apical (outer) and basolateral (inner) membranes of the polarised epithelial cells. Both apical and basolateral TFP addition induced a dose-dependent stimulation of Na transport, and depolarised the cellular potential. The data indicate that TFP acts by increasing the Na permeability of the apical membrane. However, the mechanisms localised in the apical and basolateral membranes are quite different. Basolateral TFP addition increased Na transport due to a stimulation of PGE2 synthesis, whereas apical TFP addition abolished Na inhibition of the apical Na channels, and thereby enhanced the Na transport. An acute toxic effect on the electrophysiological parameters was noted after addition of high apical TFP concentrations (50–100μM). This toxic effect was dependent on the presence of Na in the apical solution.

scholarly journals Angiotensin stimulation of bovine adrenocortical cell growth.

1977 ◽  
Vol 74 (12) ◽  
pp. 5569-5573 ◽  
Author(s):  
G. N. Gill ◽  
C. R. Ill ◽  
M. H. Simonian
Keyword(s):  
Cell Growth ◽  
Adrenocortical Cell ◽  
Stimulation Of
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