Publications by authors named "G Mazzochi"

Arginine-vasopressin (AVP) markedly increased basal aldosterone (ALDO) secretion by dispersed zona-glomerulosa (ZG) cells, and its effect was selectively reversed by V1-receptor antagonists (AVP-A1). Corticosterone (B) production by dispersed zona fasciculata (ZF) cells was not affected. The bolus intraperitoneal (i.

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The function and morphology of adrenal zona-fasciculata (ZF) mitochondria were studied in 4-, 10- and 16-month-old rats, since in this species ageing causes a marked decline in glucocorticoid secretion coupled with high levels of circulating ACTH. Dispersed intact ZF cells displayed a significant age-dependent impairment of their basal pregnenolone (PREG) secretion, but isolated ZF mitochondria showed an increased capacity to convert cholesterol to PREG (the first rate-limiting step of steroid synthesis). These data are in keeping with the contention that the age-related deficit of rat ZF secretion is located prior to the activity of intramitochondrial cholesterol side-chain cleaving enzymes (cytochrome-P450scc).

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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.

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The effects of chronic ACTH administration on adrenocortical cells autotransplanted in the rat spleen have been investigated. Morphometry showed that ACTH induced a significant hypertrophy of adrenocortical cells, which was mainly due to the increase in the smooth endoplasmic reticulum and mitochondrial compartment. Competitive protein binding assay demonstrated that adrenocortical cell hypertrophy was associated with a two-fold rise in the plasma corticosterone concentration.

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The effects of a chronic administration of angiotensin II on the zona fasciculata of rats treated with dexamethasone and maintenance doses of ACTH were investigated by morphometric methods applied to electron microscopy. It was found that angiotensin induced a significant increase in the volume of cells, nuclei, mitochondrial and lipid compartments as well as in the surface area of smooth endoplasmic reticulum and mitochondrial cristae. Noticeable also were the hypertrophy of the Golgi apparatus and the increase in the number of acid phosphatase-positive dense bodies.

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