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Biomedical subjects

G Mazzocchi

Publications and source records attributed to G Mazzocchi.

At least 109 records · Page 6Linked to original sources
PubMed1989

Effects of the infusion with ACTH or CRH on the secretory activity of rat adrenal cortex.

Six-hour infusion with ACTH or CRH induced a dose-dependent rise in the plasma concentrations of ACTH, corticosterone (B) and aldosterone (A). Positive linear correlations between the plasma levels of ACTH and B or A were found in both ACTH-or CRH-infused animals. Regression curves for B were similar in both groups of animals, while the regression line for A was significantly (P less than 0.05) steeper in CRH-than in ACTH-treated rats. These findings suggest that, in the rat, the mechanism underlying the CRH-induced stimulation of A secretion does not exclusively involve the enhancement of ACTH release.

Adrenal Cortex↗
PubMed1989

Further studies on the involvement of dopamine and somatostatin in the inhibitory control of the growth and steroidogenic capacity of rat adrenal zona glomerulosa.

Prolonged (12-day) sodium restriction increased basal plasma concentration of aldosterone and provoked a notable hypertrophy of the zona glomerulosa and its cells in rats. A 7-day infusion of dopamine or somatostatin, at a rate which was found to exert a maximum inhibition of aldosterone secretion in 12 h, only partially reversed the effects of sodium deprivation. However, the combined administration of these two molecules not only completely annulled the effects of sodium restriction, but also lowered plasma aldosterone concentration and the volumes of the zona glomerulosa and its cells below the values found in rats fed a normal diet. These findings confirm the contention that dopamine and somatostatin are both involved in the negative control of the growth and steroidogenic capacity of the rat zona glomerulosa, and suggest that different mechanisms underlie the antiadrenoglomerulotrophic action of these molecules.

Aldosterone↗
PubMed1989

Effect of subacute cabergoline treatment on prolactin, thyroid stimulating hormone and growth hormone response to simultaneous administration of thyrotrophin-releasing hormone and growth hormone-releasing hormone in hyperprolactinaemic women.

It is known that dopaminergic neurotransmission is involved in the control of PRL, TSH and GH secretion. Cabergoline (CAB) is a new ergolinic derivative with a long-acting dopaminergic activity. We evaluated 11 women with pathological hyperprolactinaemia before and during sub-acute CAB treatment (0.8-1.2 mg/p.o.; 8 weeks). Simultaneous administration of TRH (200 micrograms i.v.) and GHRH 1-44 (50 micrograms i.v.) were carried out before and after 4, 8 and 10 week intervals from the beginning of CAB treatment. Basal PRL levels (2453.5 +/- S.E. 444.5 mU/l) were significantly reduced during CAB administration (week 4: 164.5 +/- 66.5 mU/l; week 8: 168.0 +/- 66.5 mU/l; P less than 0.01) and no variations were observed 2 weeks after drug discontinuation (week 10: 210.0 +/- 98.0 mU/l). PRL percentage change after TRH was increased by CAB (P less than 0.05). No variation in basal and TRH-stimulated TSH levels was found during CAB administration. A slight increase in GH basal levels (3.0 +/- 0.6 mU/l) was found after weeks 4 (6.4 +/- 2.0 mU/l) and 10 (5.8 +/- 1.6 mU/l) (P less than 0.05). GH response to GHRH was significantly enhanced (ANOVA: P less than 0.01) during sub-acute CAB treatment. A positive correlation was found between GH secretory area and weeks of CAB therapy (P less than 0.01). Our data show that CAB is very effective in lowering PRL secretion in hyperprolactinaemia, and is able to modify PRL and GH responses after TRH and GHRH. The increasing trend in GH basal and GHRH-stimulated GH levels seems to indicate that CAB can override the central dopaminergic tone which is operative in hyperprolactinaemia.

Adult↗
PubMed1989

Effects of prolonged cyclosporine-A treatment on the morphology and function of rat adrenal cortex.

The effects of prolonged (30 day) treatment with daily therapeutical doses of cyclosporine A (CSA) (20 mg/kg) on the function and morphology of adrenal cortex were studied in adult male rats. CSA-treated animals developed a notable hypertension, along with a striking rise in PRA, which was not coupled with significant changes in the plasma concentrations of aldosterone and corticosterone (hyperreninemic hypoaldosteronism). Morphometry showed that zona glomerulosa (ZG) and zona fasciculata, and their parenchymal cells were atrophic. Isolated capsular (ZG) and inner (zona fasciculata/reticularis) cells displayed reduced basal and stimulated secretory responses. However, while the response of ZG cells to angiotensin II was almost completely suppressed (96%), basal steroid secretion of isolated cells, as well as the aldosterone and corticosterone response of ZG cells to potassium and ACTH, and corticosterone production of inner cells in response to ACTH were decreased by only about 30-40%. The hypothesis is advanced that CSA exerts a dual effect on rat adrenal cortex: 1) a general inhibitory effect on the growth and steroidogenic capacity of adrenocortical cells, which manifests itself only after very prolonged treatment and may be caused by an impairment of protein synthesis; and 2) an acute effect involving the specific blockade of the angiotensin-II-induced stimulation of the secretory activity of ZG cells.

Adrenal Cortex↗
PubMed1989

Effects of 4-aminopyrazolo (3,4-d) pyrimidine on rat hepatocytes: an ultrastructural morphometric study.

The prolonged administration of the hypolipidemic drug 4-aminopyrazolo (3,4-d) pyrimidine (4APP) induced conspicuous morphological changes in rat hepatocytes, which are clearly demonstrated by stereology. We observed a significant decrease in the rough endoplasmic reticulum, and an accumulation of lipid droplets, which was coupled with a comparable rise in the hepatic concentrations of total cholesterol and triglycerides. These changes were interpreted as the expression of the 4APP-provoked impairment of the synthesis of the polypeptide chains of lipoproteins and of the consequent suppression of the assembly of lipid molecules in exportable lipoproteins. We also noted a neto lowering in smooth endoplasmic reticulum and peroxisomes, a decrease which was hypothesized to be the morphological counterpart of a reduced de novo cholesterol synthesis, due to the 4APP-induced rise in the intracellular cholesterol concentration.

Adenine↗
PubMed1989

Growth hormone and prolactin response to growth hormone-releasing in anorexia nervosa.

Anorexia nervosa (AN) is associated with several endocrine disorders. In order to investigate the role of these alterations, growth hormone-releasing hormone (GHRH) was administered in a group of 9 AN patients and in 9 healthy normal-weight women as control. Growth hormone (GH) and prolactin (PRL) levels were evaluated in both groups after GHRH and saline solution administration. In the AN group, luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyrotropin (TSH) and cortisol serum levels were evaluated during GHRH administration; somatomedin-C (Sm-C) basal levels were also determined. In both groups, GHRH induced a prompt GH increase, which was significantly higher in AN patients (55.3 +/- 2.9 ng/ml, mean +/- SE) than in normal subjects (9.8 +/- 2.6 ng/ml: p less than 0.01). A significant positive correlation between mean GH basal values and GH peak after GHRH was observed only in the control group (R = 0.82, p less than 0.01). No significant relationship between GH mean peak and body mass index (BMI) or Sm-C, estradiol (E2) and glucose serum levels was found in AN patients. However, a positive significant correlation with triiodothyronine (T3) basal values was observed in this group (R = 0.80, p less than 0.01). Both groups showed no variation in PRL serum levels after GHRH infusion. Our data suggest the presence of a central derangement in hypothalamic control of pituitary function in patients with AN, which is not necessarily due to weight loss alone.

Adolescent↗
PubMed1989

A morphometric study of the reversal of ACTH-induced hypertrophy of rat adrenocortical cells after cessation of treatment.

The effect of a prolonged (7-day) ACTH administration on rat zona fasciculata cells and its reversal after cessation of treatment was investigated by morphometry. ACTH treatment caused a notable cell hypertrophy, which was mainly due to the increase in the volume of the mitochondrial compartment and to smooth endoplasmic reticulum (SER) proliferation, and a conspicuous rise in the basal level of corticosterone. After cessation of ACTH administration, rat zona fasciculata cells underwent a time-dependent atrophy, so that after 5 days they resembled those of control animals, and the blood concentration of corticosterone reverted to the base-line value. The cell atrophy was provoked by the decrease in the volumes of the mitochondrial compartment and SER, and was associated with a striking time-dependent accumulation of dense bodies. Stereology demonstrated that during the first two days after ACTH withdrawal the decrease of SER prevailed over that of the mitochondrial compartment, while the reverse occurred during the remaining three days. The increase in the volume of dense-body compartment, though largely due to the accumulation of residual bodies, was mainly coupled with a rise in the volume of the microautophagic-vacuole compartment during the first two days after ACTH cessation and with an increase in that of the macroautophagic-vacuole compartment during the following three days. The hypothesis is advanced that both micro- and macroautophagy play a role in the reversal of ACTH-induced hypertrophy of rat zona fasciculata cells after cessation of treatment, the first process being mainly involved in the elimination of SER, and the second one in the degradation of mitochondria.

Adrenocorticotropic Hormone↗
PubMed1989

Stereological and functional investigations on isolated adrenocortical cells. I. Adrenocortical cells of normal adult rats.

The function and morphology of isolated rat adrenocortical cells were investigated. Capsular (zona glomerulosa) cells secreted aldosterone, progesterone and small amounts of corticosterone; inner (zonae fasciculata and reticularis) cells produced corticosterone and progesterone. ACTH (10(-8) M) exposure caused a striking rise in aldosterone and corticosterone secretion by capsular cells, and in corticosterone release by inner cell preparations; simultaneously, progesterone secretion was significantly reduced. Capsular and inner cells possessed an average volume of 500 and 1250 micron 3, and ultrastructural qualitative and quantitative (stereological) features closely resembling those of zona glomerulosa and zona fasciculata-reticularis cells in situ, respectively. ACTH exposure caused a notable lipid-droplet depletion in both types of isolated cells.

Adrenal Cortex↗
PubMed1989

A stereologic study of the granule population of rat atrial myoendocrine cells: effects of chronic water/sodium restriction and acute water/sodium load.

The effects of chronic water/sodium restriction and acute water/sodium load on the "specific granule" population of rat atrial cardiocytes were investigated by stereology. The volume density (Vv) of atrial granules, which contain atrial natriuretic peptide (ANP), displayed a 135%-rise in water/sodium-restricted animals. The injection of 2.5 ml of isotonic saline to water/sodium-restricted rats provoked a striking degranulation of atrial myoendocrine cells (Vv of granules decreased by about 31%). The administration of an equal volume of hypertonic (5%) saline caused a more pronounced effect (Vv decreased by about 51%). These findings are in agreement with the view that chronic water/sodium restriction blocks the exocytotic release of atrial granules, without lowering the rate of their production. Moreover, they suggest that not only blood volume expansion, but also sodium ions can be a potent stimulating factor of ANP release.

Animals↗
PubMed1989

Morphological and functional responses of rat Leydig cells to a prolonged treatment with human chorionic gonadotropins.

The morphological and functional responses of rat Leydig cells to a 3- and 6-day treatment with human chorionic gonadotropins (hCG) (10 IU/kg/day) were investigated by morphometric and radioimmunological techniques. hCG-administration induced a notable time-dependent enhancement in the steroidogenic capacity and growth of Leydig cells; this last was almost exclusively due to hypertrophy (and not to hyperplasia). The volume of mitochondrial and peroxisome compartments, as well as the surface area per cell of mitochondrial cristae and smooth endoplasmic reticulum (SER) were significantly increased after hCG treatment, and showed a highly significant positive linear correlation with both basal and stimulated testosterone production by isolated Leydig cells of the contralateral testis. Also the volume of nuclei and lipid-droplet compartment and the surface area per cell of Golgi apparatus displayed a notable hCG-induced rise, but they did not correlate with testosterone secretion. These findings suggest that, in addition to mitochondria and SER, in which the enzymes of steroid synthesis are located, peroxisomes are also specifically involved in the secretory activity of rat Leydig cells.

Animals↗
PubMed1988

Effects of mevinolin, an inhibitor of cholesterol synthesis, on the morphological and functional responses of rat adrenal zona fasciculata to a prolonged treatment with 4-aminopyrazolo-pyrimidine.

Rat adrenocortical cells are almost completely dependent upon the continuous supply of cholesterol derived from serum lipoproteins. However, a prolonged (5-day) administration of 4-aminopyrazolo-pyrimidine (4-APP), a potent hypocholesterolaemic drug, though provoking a notable decrease in the intra-adrenal concentration of esterified and free cholesterol, did not significantly affect basal plasma level of corticosterone. Morphometry showed a conspicuous hypertrophy of zona fasciculata cells, coupled with a striking proliferation of smooth endoplasmic reticulum (SER) and peroxisomes and with a profound lipid-droplet depletion. The secretory response of zona fasciculata cells to ACTH was still present, but reduced by half with respect to control rats. The simultaneous administration of mevinolin, an inhibitor of cholesterol synthesis, to 4-APP-treated rats caused an additional drop in the intracellular content of free cholesterol and notably lowered basal plasma corticosterone concentration. Mevinolin magnified the 4-APP-induced zona fasciculata cell hypertrophy, as well as SER and peroxisome proliferation. The secretory response to ACTH was completely suppressed. These data are compatible with the view that the morphological changes, which rat zona fasciculata cells undergo during prolonged hypocholesterolaemia, are the expression of the activation of the endogenous cholesterol synthesis. This compensatory response, enabling zona fasciculata cells to maintain a normal basal rate of hormonal output and to respond (though less efficiently) to their main physiological stimulus, seems to be completely independent of any activation of the hypothalamo-hyphophyseal axis, since dexamethasone/ACTH treated rats were used. The hypothesis is advanced that the mechanism underlying this response may involve the decrease of the intracellular free-cholesterol pool.

Adenine↗
PubMed1988

Effects of prolonged dopamine infusion on the zona glomerulosa of sodium-restricted rats treated or not with prolactin: stereology and plasma hormone concentrations.

Prolonged sodium restriction was found to induce a notable hypertrophy of rat zona glomerulosa (ZG) cells and a significant rise in the basal plasma aldosterone concentration. Chronic prolactin administration significantly furthered the effects of sodium restriction. Dopamine infusion (3 mg/kg day for 7 days) did not apparently affect ZG morphology and function in the control rats, while it significantly counteracted the effects of sodium deprivation combined or not with prolactin administration. However, the action of dopamine was less intense in sodium-deprived rats treated with prolactin. These findings confirm the view that the dopaminergic system exerts a tonic inhibitory effect, modulated by the sodium balance, on the growth and secretory activity or rat ZG. Moreover, they suggest that the mechanism(s) underlying the antiadrenoglomerulotrophic action of dopamine in rats only partially involve(s) the well-known suppression of the hypophyseal release of prolactin.

Adrenal Cortex↗
PubMed1988

Effects of streptozotocin-induced experimental diabetes on the morphology and function of the zona fasciculata of rat adrenal cortex.

The effects of a severe streptozotocin (STZ)-induced diabetes on the morphology and function of the adrenal zona fasciculata were examined in rats with intact or pharmacologically interrupted hypothalamic-hypophyseal-adrenal axis. In animals with an intact hypothalamic-hypophyseal axis, STZ-diabetes induced hypertrophy of the cells of the zona fasciculata and a rise in the plasma corticosterone concentration. Conversely, in rats in which the hypothalamic-hypophyseal axis had been interrupted, experimental diabetes provoked atrophy of the zona fasciculata cells, and a lowering in the plasma corticosterone level. The effects of STZ-diabetes were completely reversed by insulin infusion in both groups of rats. The hypothesis is discussed that the chronic lack of insulin may directly inhibit the growth and steroidogenic capacity of the rat zona fasciculata and that this effect of experimental diabetes may be masked in rats with an intact hypothalamic-hypophyseal axis by the concurrent enhancement of ACTH release due to chronic stress resulting from the metabolic consequences of prolonged diabetes.

Animals↗
PubMed1988

Further investigations on the atrial natriuretic factor (ANF)-induced inhibition of the growth and steroidogenic capacity of rat adrenal zona glomerulosa in vivo.

A prolonged infusion with ANF (20 micrograms/kg/h for 7 days) induced atrophy of zona glomerulosa cells and lowering of basal plasma concentration of aldosterone in rats whose hypothalamo-hypophyseal-adrenal axis and renin-angiotensin system had been interrupted by the simultaneous administration of dexamethasone/captopril and maintenance doses of ACTH/angiotensin II. Chronic ANF treatment also caused comparable reductions in the aldosterone response of zona glomerulosa cells to the acute stimulation with angiotensin II, potassium and ACTH. These data are interpreted to indicate that ANF exerts an inhibitory effect on the growth and secretory activity of rat zona glomerulosa, and that the mechanism underlying this action of ANF does not involve blockade of renin release or ACTH secretion.

Adrenal Cortex↗
PubMed1988

Evidence that prolonged alpha-MSH infusion enhances the steroidogenic capacity of rat adrenal zona glomerulosa in vivo.

Prolonged infusion with 120 micrograms/kg/day alpha-MSH significantly increased basal plasma level of aldosterone in the rat, as well as raised the acute aldosterone response to a bolus administration of a high dose of ACTH or angiotensin II. These findings suggest that chronic alpha-MSH treatment stimulates the steroidogenic capacity of rat zona glomerulosa.

Adrenal Glands↗
PubMed1988

Evidence that long-term administration of a methionine-enkephalin analogue stimulates the growth and steroidogenic capacity of rat inner adrenocortical cells.

A prolonged infusion with D-ala2-met-enkephalinamide (DALA) caused a significant increase in both basal and ACTH-stimulated corticosterone secretion by dispersed inner adrenocortical cells of rats whose hypothalamo-hypophyseal axis was pharmacologically interrupted. This effect of DALA was associated with a notable hypertrophy of isolated cells. These findings suggest that enkephalins are involved in the stimulation of the growth and steroidogenic capacity of the cells of the inner layers of rat adrenal cortex.

Adrenal Cortex↗
PubMed1988

Long-term stimulatory effect of neuropeptide-Y on the growth and steroidogenic capacity of rat adrenal zona glomerulosa.

A prolonged infusion with neuropeptide-Y (NPY) caused a notable hypertrophy of the adrenal zona glomerulosa and its parenchymal cells in rats whose hypothalamo-hypophyseal axis and renin-angiotensin system were pharmacologically interrupted. Zona glomerulosa hypertrophy was associated with a significant rise in both basal and stimulated plasma levels of aldosterone. Zona fasciculata cells and the blood concentration of corticosterone were not affected. These findings suggest that NPY is specifically involved in the stimulation of the growth and steroidogenic capacity of rat adrenal zona glomerulosa.

Adrenal Cortex↗