Interaction of ACTH, β-endorphin and α-melanocyte stimulating hormone in relation to the corticosteroid production of isolated rat adrenocortical zona fasciculata and zona glomerulosa cells

FEBS Letters ◽  
1992 ◽  
Vol 296 (1) ◽  
pp. 87-89 ◽  
Author(s):  
Katalin Sz. Szalay ◽  
Gábor Folly
Keyword(s):  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Melanocyte Stimulating Hormone ◽  
Glomerulosa Cells ◽  
Isolated Rat ◽  
Zona Glomerulosa Cells ◽  
Stimulating Hormone

Long-term trophic action of α-melanocyte-stimulating hormone on the zona glomerulosa of the rat adrenal cortex

1986 ◽  
Vol 112 (3) ◽  
pp. 404-408 ◽  
Author(s):  
Claudia Robba ◽  
Piera Rebuffat ◽  
Giuseppina Mazzocchi ◽  
Gastone G. Nussdorfer
Keyword(s):  
Plasma Level ◽  
Adrenal Cortex ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Short Term ◽  
Melanocyte Stimulating Hormone ◽  
Glomerulosa Cells ◽  
Zona Glomerulosa Cells ◽  
Stimulating Hormone

Abstract. The effects of α-melanocyte-stimulating hormone (α-MSH) on the rat adrenal cortex were investigated by coupled morphometric and radioimmunological techniques. Short-term α-MSH administration provoked a significant increase in the aldosterone plasma level along with a notable lipid droplet depletion in zona glomerulosa cells. Long-term α-MSH treatment induced a notable hypertrophy of zona glomerulosa cells and a further rise in the blood concentration of aldosterone. α-MSH did not affect zona fasciculata morphology and corticosterone plasma level. The possibility is discussed that α-MSH may be specifically involved in the control of the growth and steroidogenic capacity of rat adrenal zona glomerulosa.

The properties of adrenal zona glomerulosa cells after purification by gravitational sedimentation

1974 ◽  
Vol 185 (1081) ◽  
pp. 375-407 ◽  
Keyword(s):  
Angiotensin Ii ◽  
Cyclic Amp ◽  
Microscopic Examination ◽  
Zona Glomerulosa ◽  
Maximal Response ◽  
Zona Fasciculata ◽  
Gravitational Sedimentation ◽  
Rat Adrenals ◽  
Glomerulosa Cells ◽  
Zona Glomerulosa Cells

The densities of latex spheres and biological cells can be reliably determined from their sedimentation rate in an albumin gradient under unit gravitational force. The densities of zona glomerulosa and fasciculata cells of rat adrenals were found to be 1.072 ± 0.004 and 1.040 ± 0.001 respectively. Purified zona glomerulosa cells of rat adrenals can be prepared by gravitational sedimentation of dispersed cells from capsule strippings of the gland, which originally contain 3 to10% zona fasciculata contamination. Electron and phase microscopic examination of the sedimented glomerulosa cells and their steroidogenic response to ACTH and cyclic AMP indicate that they are reasonably free of contamination from zona fasciculata cells. Electron microscopic examination of the purified glomerulosa cells indicates that most of them are reasonably normal in structure. Their basal production of corticosterone is decreased after sedimentation. However, their maximal response of corticosterone output to serotonin and potassium and their response to all potassium concentrations is not significantly altered, indicating normal function for the cells producing steroids. Their maximal responses to ACTH, valine angiotensin II and cyclic AMP are decreased, but, at the doses used, steroidogenesis by the zona fasciculata contamination in the unfractionated preparation would be stimulated by these substances. Purified zona glomerulosa cells have about the same maximal response of corticosterone output (about twofold) to potassium, valine and isoleucine angiotensin II, serotonin and ACTH. The maximal response of the purified zona glomerulosa cells to cyclic AMP is similar to that elicited by valine and isoleucine angiotensin II, potassium, serotonin or ACTH. This indicates that if these stimuli act by increasing cyclic AMP output, then the maximal response of corticosterone output (about twofold) is defined by the limited response of the biosynthetic pathways to cyclic AMP.

Long-term effects of ACTH combined with angiotensin II on steroidogenesis and adrenal zona glomerulosa morphology in the rat

1987 ◽  
Vol 114 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Anne M. Riondel ◽  
Piera Rebuffat ◽  
Giuseppina Mazzochi ◽  
Gastone G. Nussdorfer ◽  
Rolf C. Gaillard ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Morphological Changes ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Homogeneous Population ◽  
Long Term Treatment ◽  
Acth Treatment ◽  
Glomerulosa Cells ◽  
Zona Glomerulosa Cells

Abstract. To test the hypothesis that the trophic action of angiotensin II on the adrenal zona glomerulosa may allow a sustained stimulation of aldosterone by ACTH by preventing the morphological changes of the zona glomerulosa cells into zona fasciculata-like elements we investigated the effects in rats of a 6-day treatment with ACTH (100 μg/kg/day) alone or combined with angiotensin II (300 ng/kg/day) on corticosterone and aldosterone production and adrenal morphology. The responsiveness of both steroids to an acute ACTH dose was also studied on the last day of long-term treatment. Morphologic data showed that prolonged ACTH treatment stimulated the growth of zona glomerulosa cells, though it transformed the tubulo-lamellar cristae of mitochondria into a homogeneous population of vesicles. Angiotensin II furthered the trophic effects of ACTH but prevented the mitochondrial transformation. Despite its ability to conserve the well differentiated aspect of the zona glomerulosa cells, the administration of angiotensin II was unable to prevent the fall in the secretion of aldosterone caused by chronic ACTH treatment and its subsequent unresponsiveness to ACTH stimulation.

Downregulation of adrenal atrial natriuretic peptide receptor mRNAs and proteins by pregnancy in rats

1997 ◽  
Vol 155 (3) ◽  
pp. 523-530 ◽  
Author(s):  
P Vaillancourt ◽  
S Omer ◽  
R Palfree ◽  
DR Varma ◽  
S Mulay
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Receptor Proteins ◽  
Glomerulosa Cells ◽  
Anp Receptors ◽  
Receptor Mrnas ◽  
Zona Glomerulosa Cells ◽  
Atrial Natriuretic

The main objective of this study was to find out if the reported changes in the aldosterone-suppressant activity of atrial natriuretic peptide (ANP) during different hormonal states in rats are due to a modulation of ANP receptors. In zona glomerulosa cells, ribonuclease protection assay detected mRNAs for guanylate cyclase (GC)-coupled ANP GC-A and GC-B receptors, and for ANP C receptors, which are not coupled to GC. Western analysis using polyclonal anti-GC-A and anti-GC-B receptor antibodies revealed the presence of GC-A but not GC-B receptor proteins in zona glomerulosa cells. Pregnancy (days 7, 16 and 21), oestradiol-17 beta and progesterone decreased mRNAs for all the three ANP receptors in zona glomerulosa cells. Pregnancy decreased GC-A receptor proteins in zona glomerulosa cells, but these recovered to virgin values on day 2 postpartum. ANP receptor mRNAs in zona glomerulosa cells increased by postpartum day 2, but did not reach the values found in virgin rats. Zona fasciculata mainly contained GC-A receptor mRNA. It is concluded that ANP receptors in rat adrenal zona glomerulosa are modulated by pregnancy, oestrogen and progesterone; a decrease in ANP GC-A receptors during pregnancy might explain the accompanying decrease in the aldosterone-suppressant effects of ANP.

Roles of type I and type II isoenzymes of cyclic AMP-dependent protein kinase in steroidogenesis in rat adrenal cells

1994 ◽  
Vol 12 (2) ◽  
pp. 195-202 ◽  
Author(s):  
B J Whitehouse ◽  
D R E Abayasekara
Keyword(s):  
Cyclic Amp ◽  
Cell Function ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Type I ◽  
Type Ii ◽  
Aldosterone Production ◽  
Dependent Protein ◽  
Glomerulosa Cells ◽  
Zona Glomerulosa Cells

ABSTRACT The role played by cyclic AMP (cAMP)-dependent protein kinases (PKAs) in rat adrenal steroidogenesis has been investigated using cAMP analogues which show partial selectivity for the type I and type II PKA isoenzymes. These were aminohexylamino-cAMP (AHA-cAMP; selective for site 1 on type I PKA), N6-benzoyl-cAMP (BZ-cAMP; selective for site 2 on PKA types I and II) and 8-thiomethyl-cAMP (TM-cAMP; selective for site 1 on type II PKA). Positive cooperativity exists between the two nucleotide-binding sites, thus the presence of type I PKA was inferred when synergistic increases in corticosteroid production were obtained with AHA-cAMP plus BZ-cAMP and that of type II PKA when synergistic increases were obtained with TM-cAMP plus BZ-cAMP. The effects of AHA-cAMP, TM-cAMP and BZ-cAMP (10–100 μmol/l) on aldosterone production by glomerulosa cell preparations and corticosterone production by fasciculata/reticularis cell preparations were compared. Dose-related stimulation of steroid production was obtained with each cAMP analogue in both types of cell preparation. Experiments were performed using the cAMP analogues in combination at doses which gave minimal stimulation individually. Cells were incubated with AHA-cAMP (66 and 100 μmol/l) or TM-cAMP (15, 30 and 45 μmol/l) in the presence and absence of 15μmol BZ-cAMP/l. Synergistic responses were obtained with both analogue pairs in both cell types. The synergism ratio in fasciculata/reticularis cell preparations for the type I PKA selective pair of analogues (100 μmol AHA-cAMP/l plus 15μmol BZ-cAMP/l) was significantly higher (P<0·01) than that for the type II selective pair (45μmol TM-cAMP/l plus 15μmol BZ-cAMP/l; 7·9±1·2 (mean±s.e.m.) and 2·6±0·3 respectively). In zona glomerulosa preparations the ratio was higher (P<0·05) for the type II selective pair (1·6±0·1 for AHA-cAMP plus BZ-cAMP and 2·8±0·4 for TM-cAMP plus BZ-cAMP). The effects of 100μmol AHA-cAMP/l and 45μmol TM-cAMP/l on the response to ACTH (1 pmol/l–10 nmol/l) were examined. Synergistic responses were obtained in fasciculata/reticularis cells with both analogues in combination with low concentrations of ACTH (10 and 100 pmol/l). In zona glomerulosa cells only the addition of TM-cAMP (45 μmol/l) in combination with 10 pmol ACTH/1 gave rise to synergistic increases in aldosterone production, which suggests that there may be some compartmentalization of the cAMP-dependent pathway in these cells. The results indicate that both isoenzymes of PKA are present in rat adrenocortical cells and can play a part in the control of steroidogenesis. Type I PKA activity appears dominant in the control of zona fasciculata/reticularis cell function whereas modulation of type II PKA activity plays a more significant role in the responses of zona glomerulosa cells.

Neuropeptide Y modulates the sensitivity of the rat adrenal cortex to stimulation by ACTH

1995 ◽  
Vol 145 (2) ◽  
pp. 283-289 ◽  
Author(s):  
J P Hinson ◽  
L A Cameron ◽  
S Kapas
Keyword(s):  
Angiotensin Ii ◽  
Neuropeptide Y ◽  
Adrenal Cortex ◽  
Mammalian Species ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Steroid Secretion ◽  
Glomerulosa Cells ◽  
Zona Glomerulosa Cells

Abstract Neuropeptide Y (NPY) has been identified in nerves supplying the adrenal cortex of several mammalian species, although its function in this tissue is unknown. The present studies, employing adrenocortical cells prepared by collagenase digestion, have shown that NPY, in the absence of other stimulants, has no effect on steroid secretion by the rat adrenal over a range of peptide concentrations (10−11 to 10 −6 mol/l). However, in the presence of physiological concentrations of ACTH, which are submaximal for the stimulation of aldosterone secretion, NPY (10−6 mol/l) significantly enhanced the secretion rate of aldosterone by rat zona glomerulosa cells in response to ACTH. This effect was specific to the rat zona glomerulosa as NPY had no effect on the response to ACTH in rat zona fasciculata cells. The effect of NPY appears to be biphasic, however, as NPY significantly attenuated the steroidogenic response to supramaximal ACTH concentrations: in rat zona glomerulosa cells the aldosterone response to 10 −8 mol ACTH/l was significantly inhibited by NPY. The effect of NPY on the ACTH response appeared to be mediated by changes in the cAMP response. NPY had no effect on the steroidogenic response to potassium ions (K+), but enhanced the response to angiotensin II. NPY (10 −6 mol/l) significantly stimulated inositol 1,4,5-trisphosphate (InsP3) production although this concentration of peptide had no effect on steroid secretion. The effects of NPY on InsP3 production were additive with those of angiotensin II. These results suggest that the role of NPY in the adrenal cortex may be to regulate the sensitivity of the zona glomerulosa to peptide stimulation. Journal of Endocrinology (1995) 145, 283–289

Inhibition of corticosteroid production by sodium pentobarbitone in rat adrenocortical preparations

1993 ◽  
Vol 136 (1) ◽  
pp. 75-83 ◽  
Author(s):  
B. J. Whitehouse ◽  
S. J. Purdy ◽  
D. R. E. Abayasekara
Keyword(s):  
Intact Animal ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Steroid Production ◽  
Adrenal Cells ◽  
Glomerulosa Cells ◽  
Pituitary Adrenal Axis ◽  
Zona Glomerulosa Cells ◽  
Stimulation Of

ABSTRACT It is possible that some of the effects of sodium pentobarbitone on the hypothalamo-pituitary-adrenal axis in the intact animal may be attributable to direct actions on the adrenal cortex. The effects of the barbiturate on steroid production by rat adrenal preparations in vitro have therefore been examined. In zona glomerulosa cells, pentobarbitone inhibited basal steroid production in a dose-related fashion. For aldosterone and corticosterone, the doses required for 50% inhibition of production (IC50) were 1·2 mmol pentobarbitone/l and 3·7 mmol/l respectively. Steroidogenesis was inhibited at lower levels of pentobarbitone in the presence of 1 nmol ACTH/l (IC50 = 0·5 mmol pentobarbitone/l for aldosterone and 2·2 mmol/l for corticosterone). In zona fasciculata/reticularis cells, production of corticosterone was similarly reduced with an IC50 of 2·8 mmol pentobarbitone/l for basal production and 1·3 mmol/l for ACTH-stimulated production. The dose-related increases in corticosterone production produced by ACTH (0·1–1000 pmol/l) or dibutyryl cyclic AMP (0·1–1·0 mmol/l) were also eliminated in the presence of 2 mmol pentobarbitone/l. The effects of pentobarbitone (1–4 mmol/l) on the production of pregnenolone and deoxycorticosterone (DOC) were also studied. In zona fasciculata/reticularis cells, the responses of both pregnenolone and DOC were bell-shaped with increases at 1 mmol pentobarbitone/l, which fell back to control levels at 4 mmol pentobarbitone/l. Stimulation of DOC, accompanied by decreases in aldosterone and corticosterone production, was also seen in zona glomerulosa cells at 1 mmol pentobarbitone/l. The effect of 1 mmol pentobarbitone/l on the conversion of 22(R)-hydroxycholesterol (5-cholestene-3β,22(R)-diol), pregnenolone, progesterone and DOC to corticosterone and aldosterone by zona glomerulosa preparations was studied. There was a comparable reduction in the conversion of these precursors (2 μmol/l) to aldosterone with yields decreased to 20–30% of those found in the absence of pentobarbitone. The dose required for 50% reduction of the conversion of progesterone (2 μmol/l) to aldosterone was 0·55 mmol pentobarbitone/l and for corticosterone the dose was 1·75 mmol pentobarbitone/l. The results obtained show that pentobarbitone is an effective inhibitor of corticosteroid biosynthesis in rat adrenal cells, and suggest that its effects are brought about by inhibition of cytochrome P450-mediated hydroxylations. Journal of Endocrinology (1993) 136, 75–83

Potassium-induced aldosterone biosynthesis in cultured rat zona glomerulosa cells

1989 ◽  
Vol 256 (4) ◽  
pp. E475-E482
Author(s):  
J. Muller ◽  
M. Lauber ◽  
C. Schmid
Keyword(s):  
Molecular Mechanisms ◽  
Primary Cultures ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
High Potassium ◽  
Primary Monolayer ◽  
Glomerulosa Cells ◽  
Potassium Restriction ◽  
Zona Glomerulosa Cells

Rat adrenal zona glomerulosa cells lost their ability to produce aldosterone from either endogenous precursors or added deoxycorticosterone within 2 days of primary monolayer culture in a medium with a potassium concentration of 6.3 mmol/l. The lost corticosterone methyl oxidase I and II activities were totally regenerated when the ambient potassium concentrations was raised to 31 mmol/l. The conversions of deoxycorticosterone to 18-hydroxycorticosterone and aldosterone were completely restored by culture in a high-potassium medium also in zona glomerulosa cells of rats in which aldosterone biosynthesis had been suppressed by potassium restriction and sodium loading. However, these conversions were not induced in zona fasciculata-reticularis cells. The induction of aldosterone biosynthesis was associated with the appearance of a mitochondrial 49,000 protein cross-reacting with an antibody raised against bovine adrenal cytochrome P-450(11) beta. Thus primary cultures of zona glomerulosa cells are promising models for studying in vitro the molecular mechanisms of long-term adaptation of aldosterone biosynthesis to sodium and potassium intake.

LACK OF EFFECT OF ANGIOTENSIN ON LEVELS OF CYCLIC AMP IN ISOLATED ADRENAL ZONA GLOMERULOSA CELLS FROM THE RAT

1981 ◽  
Vol 91 (1) ◽  
pp. 145-154 ◽  
Author(s):  
J. B. G. BELL ◽  
J. F. TAIT ◽  
S. A. S. TAIT ◽  
G. D. BARNES ◽  
B. L. BROWN
Keyword(s):  
Angiotensin Ii ◽  
Bovine Serum Albumin ◽  
Cyclic Amp ◽  
Phosphodiesterase Inhibitor ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Angiotensin Iii ◽  
Independent Mechanism ◽  
Glomerulosa Cells ◽  
Zona Glomerulosa Cells

The effects of pure [Asp1, Val5]- and [Asn1, Val5]-angiotensin II and also [des-Asp1, Ile5]-angiotensin II (angiotensin III) on cyclic AMP and steroid outputs by dispersed rat capsular cells, comprising 95% zona glomerulosa and 5% zona fasciculata cells, have been studied. The results showed that [Asp1, Val5]- and [Asn1, Val5]-angiotensin II, at doses between 2·5 × 10−1 1 and 2 × 10−4 mol/l, which produced typical increases in steroidogenesis, failed to increase output of cyclic AMP. This lack of effect was observed whether the nucleotide was measured by radioimmunoassay or by adrenal binding protein and under the same conditions in which 8·4 mm-K+ consistently increased the output of cyclic AMP. Instead the results showed a small but significant decrease in cyclic AMP output with angiotensin II. Similar results were obtained with incubations for 60 rather than 120 min and with medium containing a concentration of 5 or 40 g bovine serum albumin/l. Although the levels of cyclic AMP were generally higher in the presence of the phosphodiesterase inhibitor, 3-isobutyl-l-methylxanthine, the same decrease relative to basal outputs was observed with angiotensin II which increased steroidogenesis. Angiotensin III also failed to increase output of cyclic AMP at doses (2·5×10−9 to 2·5×10−6 mol/l) which produced increases in steroid output equivalent to those obtained with angiotensin II. These results indicate that angiotensin II and III can act through a cyclic AMP- independent mechanism.

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