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P Rebuffat

Publications and source records attributed to P Rebuffat.

At least 91 records · Page 5Linked to original sources
PubMed1987

Effect of long-term inhibition of hydroxy-methylglutaryl coenzyme A reductase by mevinolin on the zona fasciculata of rat adrenal cortex. A combined morphometric and biochemical study.

The effects of a 7-day infusion with mevinolin, a potent competitive inhibitor of hydroxy-methylglutaryl coenzyme A (HMG-CoA) reductase, on the adrenal zona fasciculata were examined in normal and dexamethasone/ACTH-treated rats. In both groups of animals, the drug caused a lowering in plasma and intra-adrenal cholesterol concentrations, as well as a slight decrease in the blood level of corticosterone. Morphometry of zona fasciculata cells showed that specific mevinolin-induced changes (i.e. those occurring in both groups of rats and therefore not due to enhanced release of ACTH following decrease in circulating corticosterone) are severe lipid-droplet depletion and a conspicuous increase in smooth endoplasmic reticulum (SER) and peroxisomes. The hypothesis is discussed that these morphological changes express a compensatory response of zona fasciculata cells to counteract the mevinolin-induced inhibition of cholesterol synthesis in both liver and adrenal cortex.

Adrenal Cortex↗
PubMed1987

Atrial natriuretic factor (ANF) inhibits the growth and the secretory activity of rat adrenal zona glomerulosa in vivo.

A prolonged infusion with ANF induced atrophy of zona glomerulosa cells of rat adrenals and lowering of plasma concentration of aldosterone, without provoking significant changes in PRA. It also notably reduced the rise in the aldosterone plasma level caused by the acute stimulation with angiotensin II. Zona fasciculata cells and the blood concentration of corticosterone did not display any significant change. These findings are interpreted to indicate that ANF exerts an inhibitory effect on the growth and secretory activity of rat zona glomerulosa.

Adrenal Glands↗
PubMed1987

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

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 micrograms/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.

Adrenal Glands↗
PubMed1987

An ultrastructural morphometric study of the effects of chronic melatonin administration on the zona fasciculata of rat adrenal cortex.

The effects of a long-term administration of melatonin on the adrenal zona fasciculata were investigated both in 'normal' rats and in animals whose hypothalamo-hypophyseal-adrenal axis had been interrupted by a prolonged infusion with dexamethasone or dexamethasone plus maintenance doses of ACTH. In the 'normal' rats, melatonin caused a notable atrophy of zona fasciculata cells, coupled with a significant lowering in the plasma concentration of corticosterone. On the contrary, in dexamethasone- or dexamethasone plus ACTH-infused animals, melatonin induced an evident hypertrophy of zona fasciculata cells which, however, was not associated with a rise in the corticosterone blood level. The hypothesis is advanced that the direct stimulatory effect of melatonin on the growth of zona fasciculata in 'normal' rats can be masked by the concurrent inhibition of the hypophyseal release of ACTH. The possible mechanism of the direct effect of melatonin on the zona fasciculata is discussed in the light of evidence indicating that this hormone enhances the intracellular catabolism of corticosterone, which is well-known to exert a powerful direct depression of the growth and steroidogenic capacity of rat adrenocortical cells.

Adrenal Cortex↗
PubMed1986

Short- and long-term effects of ACTH on the adrenal zona glomerulosa of the rat. A coupled stereological and enzymological study.

Short-term ACTH treatment provoked a decrease in volume of the lipid-droplet compartment in rat zona glomerulosa cells, and a rise in plasma and intracellular concentrations of corticosterone and aldosterone. It enhanced activities of 3 beta-hydroxysteroid dehydrogenase (3 beta HSD), 11 beta-hydroxylase (11 beta OH) and 18-hydroxylase (18OH). Long-term ACTH administration produced a hypertrophy of the zona glomerulosa and its parenchymal cells, a result of the increase in volume of the smooth endoplasmic reticulum and the mitochondrial compartment. The surface area per cell of mitochondrial inner membranes increased; the tubular cristae were transformed into a homogeneous population of vesicles. The plasma and intracellular concentrations of corticosterone further increased, whereas those of aldosterone fell below basal levels (the "aldosterone-escape" phenomenon). The activities of 3 beta HSD and 11 beta OH were enhanced, that of 180H decreased. Therefore, ACTH stimulates zona glomerulosa growth and transforms parenchymal elements into zona fasciculata cell-types. Cyanoketone nullified acute ACTH effects on plasma and intracellular concentrations of corticosterone and aldosterone, but did not affect the activities of 11 beta OH and 18OH. Chronic ACTH treatment produced similar results, although 18OH activity was not suppressed. The mechanism underlying the "aldosterone-escape" phenomenon may thus involve a rise in the intracellular concentration of corticosterone, caused by the enhanced synthesis and activation of 3 beta HSD and 11 beta OH.

3-Hydroxysteroid Dehydrogenases↗
PubMed1986

Further studies on the effects of prolonged prolactin administration on the zona glomerulosa of the rat adrenal cortex.

The effects of a prolonged treatment with prolactin on the morphology and hormone secretion of adrenal zona glomerulosa of gonadectomized testosterone-replaced rats were investigated by coupled morphometric and radioimmunologic techniques. The dexamethasone/captopril-induced atrophy of zona glomerulosa cells (-42%) and fall in the blood level of aldosterone (-37%) were partially counteracted by chronic prolactin administration: the values had increased by about 15% and 17%, respectively, but remained lower than in the control animals. The prolonged treatment with prolactin of dexamethasone/captopril-administered ACTH/angiotensin II-replaced rats provoked a striking increase in the zona glomerulosa cell volume (24%) and in the blood level of aldosterone (33%) above the control values. The possibility is discussed whether prolactin may be directly involved in the stimulation of the growth and steroidogenic capacity of rat zona glomerulosa, without interacting with the gonads and interfering with the hypothalamo-hypophyseal axis and the renin-angiotensin system.

Adrenal Cortex↗
PubMed1986

Investigations on the effects of long-term administration of a methionine-enkephalin analogue on the adrenal zona fasciculata of rats treated with dexamethasone or dexamethasone and ACTH.

Prolonged (7 days) methionine-enkephalin (DALA) treatment provoked a dose-dependent increase in the volume of zona fasciculata cells of dexamethasone-administered rats, along with a notable rise in the plasma concentration of corticosterone and the activity of 11 beta-hydroxylase. Comparable dose-dependent effects were observed after chronic administration of ACTH to dexamethasone-suppressed rats. The chronic administration of the maximum dose of DALA (500 micrograms/kg/day) was found to significantly further the trophic action of ACTH on the zona fasciculata of dexamethasone-treated animals. It is suggested that enkephalins act independently of and synergistically with ACTH in stimulating the growth and steroidogenic capacity of the rat adrenal zona fasciculata.

Adrenal Cortex↗
PubMed1986

Short- and long-term effects of angiotensin II on the rat adrenal zona glomerulosa. A coupled stereological and enzymological study.

Long-term angiotensin II administration induced a time-dependent increase in the volume of rat zona glomerulosa cells and in the plasma concentration of aldosterone. Cell hypertrophy is coupled with comparable increases in the surface area per cell of mitochondrial cristae and in the activity per cell of 18-hydroxylase. 11 beta-hydroxylase activity was not affected. These findings allow to suggest that the angiotensin-II-enhanced growth of rat zona glomerulosa is associated with the de novo synthesis of 18-hydroxylase.

Adrenal Cortex↗
PubMed1986

Effects of prolactin administration on the zona glomerulosa of the rat adrenal cortex: stereology and plasma hormone concentrations.

The effects of short and prolonged treatments with prolactin on the morphology and hormone secretion of the rat adrenal zona glomerulosa were investigated by coupled morphometric and radioimmunological techniques. Short-term prolactin administration did not alter plasma aldosterone concentration or zona glomerulosa morphology. Conversely, chronic prolactin treatment caused both a notable hypertrophy of zona glomerulosa cells and a significant rise in the blood level of aldosterone. The possibility is discussed that prolactin may be involved in the control of the growth and steroidogenic capacity of the rat adrenal zona glomerulosa.

Adrenal Cortex↗
PubMed1986

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

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

Adrenal Cortex↗
PubMed1985

Effect of somatostatin on the zona glomerulosa of rats treated with angiotensin II or captopril: stereology and plasma hormone concentrations.

Chronic somatostatin (SRIF) administration induced atrophy of zona glomerulosa cells of the rat adrenal cortex and a noticeable fall in the plasma concentration of aldosterone. The effects of SRIF were comparable with those of captopril, a specific inhibitor of the angiotensin-converting enzyme. SRIF completely abrogated the adrenoglomerulotrophic effects of angiotensin II (AII); the inhibitory actions of SRIF and captopril were not additive. The slight but significant enhancement of zona fasciculata cell growth and plasma corticosterone levels caused by chronic AII administration were ot reversed by SRIF. We interpret these data to indicate that SRIF specifically modulates the stimulatory effects of AII on the growth and steroidogenic capacity of rat zona glomerulosa.

Adrenal Cortex↗
PubMed1985

Trophic effects of potassium loading on the rat zona glomerulosa: permissive role of ACTH and angiotensin II.

The trophic effects of chronic potassium loading on the rat zona glomerulosa were investigated by morphometric and radioimmunological methods. Potassium loading exerted a potent adrenoglomerulotrophic effect in saline treated control rats, but it was not able to reverse the captopril- and dexamethasone-induced atrophy of the zona glomerulosa. However, if the captopril/dexamethasone administered rats were given maintenance doses of angiotensin II and ACTH, potassium loading was found to exert a strong trophic action. The hypothesis is advanced that potassium loading requires the integrity of both the renin-angiotensin system and the hypothalamo-hypophyseal axis to exert its powerful direct stimulating effect on the growth and steroidogenic capacity of the rat zona glomerulosa.

Adrenal Glands↗
PubMed1985

Opposed effects of chronic prolactin administration on the zona fasciculata and zona reticularis of the rat adrenal cortex: an ultrastructural stereological study.

The effects of a prolonged treatment with prolactin on the morphology and hormone secretion of rat adrenal zona fasciculata and zona reticularis, were investigated by coupled morphometric and radio-immunological techniques. Chronic prolactin administration provoked a notable atrophy of zona fasciculata cells and a small but significant increase in the corticosterone plasma level, which can be the result of the prolactin-induced inhibition of the intra-adrenal 5 alpha-reductase. Therefore, the atrophy of the zona fasciculata may be reasonably supposed to be not a direct effect of prolactin, but indirectly caused by a negative feed-back mechanism blocking ACTH release. On the contrary, prolonged prolactin treatment induced a conspicuous hypertrophy of zona reticularis cells, as well as a notable rise in the plasma concentration of testosterone, which cannot be due to gonad stimulation by prolactin since orchiectomized rats were employed. As the zona reticularis, like zona fasciculata, is ACTH-dependent, it must be concluded that prolactin exerts a direct stimulating effect on the growth of the zona reticularis, whose functional counterpart conceivably is an enhanced production of androgen hormones.

Adrenal Cortex↗
PubMed1984

Inhibitory effect of somatostatin on the growth and steroidogenic capacity of rat adrenal zona glomerulosa.

Chronic administration of somatostatin induced atrophy of zona glomerulosa cells of rat adrenals and lowering of plasma aldosterone concentration. Zona fasciculata cells did not display any significant change and corticosterone plasma concentration was not significantly affected. These findings are interpreted to indicate that somatostatin exerts a direct inhibitory effect on the growth and steroidogenic capacity of rat adrenal zona glomerulosa.

Adrenal Cortex Hormones↗
PubMed1983

Morphometric investigations into the mechanism of the compensatory hypertrophy of the rat adrenal zona fasciculata after unilateral adrenalectomy.

Compensatory hypertrophy of the remaining gland in unilaterally adrenalectomized rats was investigated by morphometric techniques. It was observed that compensatory adrenal growth occurred in both dexamethasone-treated and hypophysectomized rats, receiving maintenance doses of ACTH. However, it was only half that found in intact animals. These results support the view that activation of the hypothalamo-hypophyseal axis is not the unique mechanism underlying adrenal compensatory hypertrophy in the rat.

Adrenal Glands↗
PubMed1983

Effects of testosterone on the zona fasciculata of the male rat adrenal cortex. A correlated stereological and biochemical study.

The effects of long-term testosterone administration on the adrenal cortex of male rats were investigated by coupled morphometric and biochemical methods. Morphometry showed that testosterone treatment provoked a time-dependent atrophy of the zona fasciculata cells, which was mainly due to the decrease in the volume of the mitochondrial compartment and smooth endoplasmic reticulum (SER). Biochemical assays demonstrated that the decrease in the surface area per cell of SER membranes and mitochondrial cristae was tightly paralleled by the decrease in the activity per cell of two key enzymes of steroid synthesis contained in them (delta 5-3 beta-hydroxysteroid dehydrogenase and 11 beta-hydroxylase). The testosterone-induced inhibition of the growth maintenance and steroidogenic capacity of adrenocortical cells provoked a significant fall in the plasma concentration of corticosterone and a consequential increase in the level of circulating ACTH. Chronic administration of testosterone caused a notable suppression of the activity of the adrenal 5 alpha-reductase and this in turn provoked a rise in the intracellular concentration of corticosterone. Moreover, testosterone inhibited the incorporation of 3H-uridine into the nuclear and mitochondrial fractions of male rat adrenocortical cells. These findings exclude the possibility that the testosterone-provoked atrophy of the male rat adrenal glands is mediated by the suppression of the hypothalamo-hypophyseal axis, and suggest that the mechanism underlying this action of testosterone involves inhibition of nuclear and mitochondrial RNA synthesis. Whether this effect of testosterone is directly or indirectly mediated by the rise in the intracellular content of corticosterone due to the inhibition of 5 alpha-reductase activity, remains to be elucidated.

3-Hydroxysteroid Dehydrogenases↗
PubMed1982

Effects of the hypolipidemic drug nafenopin on the zona fasciculata of the rat adrenal cortex: a correlated biochemical and stereological study.

The effects of Nafenopin, a hypolipidemic drug, on the zona fasciculata of the rat adrenal cortex were investigated by biochemical, stereological, and cytochemical methods. Chronic Nafenopin treatment (5 days) significantly lowered serum cholesterol level, while it did not alter blood corticosterone concentration and 11beta-hydroxylase activity of adrenocortical cells. Stereology showed a significant increase in the average volume of zona fasciculata cells, which was almost exclusively due to smooth endoplasmic reticulum (SER) proliferation. The volume of lipid compartment was significantly reduced, whereas the volume of diaminobenzidine (DAB)-positive bodies (peroxisomes) per cell displayed a marked increase. Cholesterol administration per os to the treated animals raised the serum cholesterol level and completely reversed the Nafenopin effects. One day of Nafenopin administration provoked a slight but significant lipid depletion in adrenocortical cells, while 3 days of continuous drug treatment induced an extreme lipid depletion and a moderate increase in the SER coupled with a significant decrease in the plasma concentration of corticosterone. Since microsomal fraction and catalase seem to be involved in the cholesterol metabolism and utilization, the hypothesis is advanced that the Nafenopin-elicited SER and peroxisome proliferation is a compensatory response enabling adrenocortical cells to maintain an adequate level of hormonal output.

Adrenal Cortex↗