Biomedical subjects

G Mazzocchi

Publications and source records attributed to G Mazzocchi.

At least 163 records · Page 9Linked to original sources

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

Effects of chloramphenicol on the long term trophic action of ACTH on rat adrenocortical cells: a combined stereological and enzymological study.

Chronic chloramphenicol administration was found to block the ACTH-induced increase in both the surface area of mitochondrial cristae and the activity of 11 beta-hydroxylase in zona fasciculata cells of the rat adrenal cortex. The surface area of agranular endoplasmic reticulum membranes and the activity of 3 beta-hydroxysteroid dehydrogenase were not affected by treatment with chloramphenicol. These findings suggest that the mechanism of the ACTH-induced enhancement of the growth and steroidogenic capacity of rat adrenocortical cells involves stimulation of mitochondrial DNA-dependent protein synthesis.

3-Hydroxysteroid Dehydrogenases↗

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

Multicentric experience on the acute effect of nomifensine in hyperprolactinemic women.

The inhibitory effect of nomifensine ( Nom ; 200 mg orally) on prolactin (PRL) secretion was studied in 15 subjects with puerperal hyperprolactinemia and in 59 pathologic hyperprolactinemic women. The latter were grouped as follows: i) patients with surgically proven PRL secretory pituitary adenomas (proven tumors; 27 cases); ii) patients presenting radiological signs of sella indicative of a pituitary tumor (presumptive tumors; 10 cases); iii) subjects with non-drug induced hyperprolactinemia (hyperprolactinemia of uncertain etiology; 22 cases). A mean PRL fall of 30% or more of baseline hormone levels in samples collected within the 120-240 min post-treatment interval was adopted to define responsiveness to Nom . In 24 out of 27 subjects with proven tumors and in 9 out of 10 subjects with presumptive tumors Nom did not induce significant variations in PRL secretion. In only 11% of the patients with surgery-confirmed or highly suspected tumors a hormone decrease greater than 30% was observed. In addition, 13 subjects with hyperprolactinemia of uncertain etiology did not respond to Nom administration. In 5 of these, additional data suggesting the existence of an adenoma were collected. Finally, 3 out of 9 Nom -responder patients presented either a polycystic ovary syndrome or transitory hyperprolactinemia. The finding that hyperprolactinemic women, who did not show clinical or radiological signs of a tumor and patients with highly presumptive or proven pituitary tumors may present comparable responses to Nom , suggests that this pattern may be indicative of an early manifestation of a PRL-secreting adenoma which has yet to evolve. The follow-up of Nom -non-responder hyperprolactinemic subjects who did not show clinical signs of harboring a tumor, is therefore advisable.

Adolescent↗

PubMed1984

Variations of thyroid hormones during total fasting in obese and in obese diabetic subjects.

Fasting and hypocaloric diets are known to induce a reduction of triiodothyronine (T3) and to increase reverse triiodothyronine (rT3) in normal and obese subjects. The effect of 8-day fasting was evaluated on T3, thyroxine (T4), free T4, rT3, TSH, immunoreactive insulin (IRI), thyroxine binding globulin (TBG) and glycemia in 21 obese subjects (5 males, 16 females) grouped according to the average starting blood glucose concentration in: group I, diabetic obese subjects (9 patients); group II, non diabetic obese subjects (12 patients). All patients had no history of recent weight loss due to dietetic therapy or drugs. Blood samples were drawn in the morning at 0, 2, 4, 6, 8 days after total caloric deprivation and 2 days after refeeding. A superimposable variation of weight and glucose concentration were seen in both groups. In addition, no difference was observed in ketone body excretion, SH, TBG, T4, free T4. In group II a significant decrease of IRI was observed during diet (p less than 0.05); T3 decreased (p less than 0.01) and rT3 increased (p less than 0.01) significantly. No variations in T3 and rT3 values were observed in group I. These results are consistent with a possible role of glucose metabolism in the genesis of the low T3 syndrome.

Adult↗

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↗

PubMed1984

Long-term effects of captopril on the morphology of normal rat adrenal zona glomerulosa. A morphometric study.

The effects of a long-term administration of captopril (Squib 14225) on the rat zona glomerulosa were investigated. Morphometry showed that this drug, which specifically inhibits angiotensin-converting enzyme, induces a notable atrophy of zona glomerulosa cells, which is principally due to the decrease in the volume of mitochondrial compartment and smooth endoplasmic reticulum. Radioimmunological assays disclosed that in the treated rats the plasma aldosterone concentration is significantly lowered. The suppressive effects of captopril were completely reserved by chronic treatment with angiotensin II. These findings confirm the view that the renin-angiotensin system is involved in the maintenance of the growth and steroidogenic capacity of the normal rat zona glomerulosa.

Adrenal Glands↗

PubMed1984

Effects of GRF(1-40) and domperidone on GH secretion in normal man.

In eight normal adult men pituitary secretion following GRF(1-40) was studied. GRF administration (50 micrograms i.v.) was followed by an increase in GH release with a peak value between the 15 and 60 min. No effects were noticed on LH, FSH, PRL, TSH and ACTH secretion. GH and PRL release was also studied after domperidone (DOM) (5 mg i.v./h), and GRF plus DOM. PRL increased significantly after DOM and GRF plus DOM. During GRF plus DOM a more marked GH release was observed in comparison with the hormone response to GRF alone at 15-45 and 120 min (P less than 0.05). This phenomenon was found in in six out of eight subjects studied. Mean peak and secretory area was greater (P less than 0.05) after GRF plus DOM than after GRF alone. These data suggest that GRF(1-40) at the dose used is a useful tool in the study of GH secretion. The GH pattern during GRF plus DOM seems to indicate that dopaminergic tone may play a direct inhibitory role on GH secretion in man.

Adolescent↗

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

Nomifensine decreases the thyroid-stimulating-hormone response to thyrotropin-releasing-hormone in normal subjects.

The Thyroid-stimulating-hormone (TSH) secretion has been studied in 12 normal euthyroid subjects (4 males, 8 females) after nomifensine (NOM) administration (200 mg po). NOM is a drug which activates dopaminergic neurotransmission at the Central Nervous System level. Blood samples were drawn every h for 4 h after NOM or placebo, respectively. At the 4th hour thyrotropin-releasing-hormone (TRH) was administered in bolus (200 micrograms iv), in both studies, and additional samples were collected for 90 min. The results show a moderate suppression (NS) of TSH and a clear-cut reduction in the secretory response to TRH after NOM administration (secretory area: TRH after placebo 723 +/- 132, TRH after NOM 400 +/- 83; p less than 0.01). The data appear to confirm that dopaminergic neurotransmission exerts an inhibitory role upon TSH secretion. The mechanism by which NOM induced dopaminergic activation leads to the suppression of TSH release after TRH has not yet been elucidated. An interference in TSH storage and/or in the post receptor mechanisms involved in TRH action might be hypothesized.

Adult↗

PubMed1983

Long-term effects of ACTH on rat adrenocortical cells: a coupled stereological and enzymological study.

The effects of a long-term ACTH administration on the morphology of rat adrenocortical cells and the activity of some enzymes of steroid synthesis contained in them were examined by stereological and biochemical techniques. It was demonstrated that ACTH provokes time-dependent increases in the surface area per cell of smooth endoplasmic reticulum and mitochondrial cristae, which are tightly parallelled by enhancements in the activity per cell of delta 5-3 beta-hydroxysteroid dehydrogenase and 11 beta-hydroxylase, respectively.

3-Hydroxysteroid Dehydrogenases↗

PubMed1983

The effect of nomifensine on thyroid-stimulating hormone (TSH) in normal and hyperprolactinemic subjects.

Thyroid-stimulating-hormone (TSH) secretion was studied in 28 normal subjects (12 males; 16 females) and in 8 subjects with prolactin (PRL) secreting tumors (1 male; 7 females) after nomifensine (NOM) administration (200 mg orally). NOM is a drug which activates dopaminergic (DA) neurotransmission at the central nervous system level. Blood samples were drawn every hour for 4 h after NOM or placebo administration. On the 4th h thyrotrophin-releasing-hormone (TRH) was administered in bolus (200 micrograms i.v.), to both groups, and additional samples were collected at 10-, 20-, 30-, 60- and 90-min intervals. The results indicate that in normal subjects, but not in prolactinomas, NOM induces a moderate but significant reduction in TDH secretion. Furthermore, the TSH response to TRH was found to be significantly reduced. No variation was discerned, however, in PRL secretion after NOM. The hormone response to TRH remained unaffected. The data confirm that in normal subjects the DA neurotransmission exerts an inhibitory role upon TSH secretion. In subjects affected by prolactinomas, an alteration in central DA availability may be hypothesized.

Adult↗

PubMed1983

Participation of endogenous opiates in regulation of the hypothalamic-pituitary-testicular axis in normal men.

To assess the influence of endogenous opioids on human gonadotropin secretion, integrated concentrations of gonadotropins during 24-h naloxone infusion (2.08 mg/h) were examined in a group of six normal men. Naloxone significantly stimulated LH secretion in all subjects, whereas serum FSH levels were similar during both saline and naloxone infusion. Serum testosterone, dihydrotestosterone, and 17 alpha-hydroxyprogesterone levels increased during the infusion of naloxone, but the delta 4-androstenedione concentration was not modified. The frequency and amplitude of LH secretory episodes were clearly increased when an equal amount of the drug was given and LH concentrations were measured every 15 min for 6 h. The results suggest the endogenous opioids inhibit the hypothalamic-pituitary-gonadal axis in normal men.

17-alpha-Hydroxyprogesterone↗

PubMed1983

Effects of angiotensin II on the zona glomerulosa of sodium-loaded dexamethasone treated rats administered or not with maintenance doses of ACTH: stereology and plasma hormone concentrations.

The trophic effects of angiotensin II on the rat zona glomerulosa were investigated by stereological and radioimmunological methods. Angiotensin II was not able to reverse the sodium-loading and dexamethasone-induced inhibition of the growth and steroidogenic capacity of the zona glomerulosa. However, if the sodium-loaded dexamethasone-treated rats were given maintenance doses of ACTH, angiotensin II exerted a strong adrenoglomerulotrophic effect. The hypothesis is advanced that the co-operation of ACTH and angiotensin II is required in the maintenance of the morphologic and enzymatic integrity of the rat zona glomerulosa.

Adrenal Glands↗

PubMed1983

Investigations of the turnover of adrenocortical mitochondria. XVI. Effects of ethidium bromide on the ACTH-induced elongation of the half-life of rat zona fasciculata mitochondria.

ACTH significantly increases the half-life of rat zona fasciculata mitochondria. Since ethidium bromide inhibits this effect of ACTH, the hypothesis is advanced that the ACTH-induced slowing-down of the degradation rate of adrenocortical mitochondria involves mitochondrial DNA reduplication and transcription.

Adrenal Cortex↗

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↗

PubMed1982

An electron-microscopic stereological study of the compensatory hypertrophy of the rat adrenal zona fasciculata after unilateral adrenalectomy.

The ultrastructural changes associated with the compensatory hypertrophy of the zona fasciculata cells on monoadrenalectomized rats were investigated by stereological techniques. It was found that these subcellular changes display a different pattern from those underlying the ACTH-induced adrenocortical cell growth in the intact rats. This result supports the view that compensatory adrenal hypertrophy does not involve activation of the hypothalamo-hypophyseal-adrenal axis.

Adrenal Cortex↗