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Biomedical subjects

G Mazzocchi

Publications and source records attributed to G Mazzocchi.

At least 235 records · Page 13Linked to original sources
PubMedDate not supplied

Effects of substance P on the rat adrenal zona glomerulosa in vivo.

Substance P (SP) acutely enhanced the plasma concentration of aldosterone in rats whose hypothalamo-hypophyseal-adrenal axis and renin-angiotensin system were pharmacologically interrupted. The maximal response was obtained with a dose of 100 micrograms/kg. A prolonged (7 days) subcutaneous infusion with SP (50 micrograms/kg/hr) caused a notable hypertrophy of zona glomerulosa cells associated with significant rises in both basal and angiotensin-stimulated plasma levels of aldosterone. Zona fasciculata and the blood concentration of corticosterone were not affected. These findings suggest that SP is specifically involved in the stimulation of the growth and secretory activity of the rat zona glomerulosa.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Endothelin-1 acutely stimulates the secretory activity of rat zona glomerulosa cells.

A bolus IV injection of endothelin-1 (ET-1) (0.5 microgram.kg-1) decreased PRA, without affecting plasma aldosterone (A) concentration. ET-1 exerted a dose-dependent stimulation of basal secretion of A and corticosterone (B) by dispersed zona glomerulosa (ZG) cells, while it did not affect B production by inner adrenocortical cells. ET-1 notably enhanced the secretory response of dispersed ZG cells to a maximal effective concentration of ACTH, but not of either angiotensin II (ANG-II) or potassium. The conclusion is drawn that ET-1 acutely stimulates ZG in rats, by a mechanism probably similar to that underlying the adrenoglomerulotropic actions of ANG-II and potassium.

Aldosterone↗
PubMedDate not supplied

Effects of prolonged infusion with endothelin-1 on the function and morphology of rat adrenal cortex.

A week of SC infusion with endothelin-1 (ET-1) (0.2 microgram.kg-1.hr-1) lowered PRA and raised plasma aldosterone (A) concentration in rats. Kalaemia and the plasma levels of ACTH and corticosterone (B) were not affected. Prolonged ET-1 administration caused a notable hypertrophy of zona glomerulosa (ZG) and its parenchymal cells, without inducing any apparent change in zona fasciculata. Stereology showed that ZG cell hypertrophy was mainly due to the increase in the volume of the mitochondrial compartment and to the proliferation of smooth endoplasmic reticulum (i.e., the two organelles in which the enzymes of steroid synthesis are contained). Isolated ZG cells from ET-1-infused animals evidenced a notable enhancement in their basal production of A and B. The secretory responses of ZG cells to the maximal effective concentrations of their three main stimulators (ACTH, angiotensin-II and K+) displayed comparable increases. These findings indicate that ET-1, when chronically administered, is able to specifically enhance the growth and steroidogenic capacity of rat ZG, and suggest that the mechanism underlying this ET-1 effect involves stimulation of the de novo synthesis of both the steroidogenic enzymes and the membrane framework in which they are located.

Adrenal Cortex↗
PubMedDate not supplied

Effect of atrial natriuretic factor (ANF) on the secretory activity of zona glomerulosa in sodium-restricted rats.

Prolonged (12-day) sodium deprivation strikingly raised both basal plasma aldosterone concentration (PAC) (114%) and plasma renin activity (PRA) (200%), and lowered ANF blood level (-30%). Acute ANF bolus administration produced a dose-dependent decrease in PAC in both normally-fed and sodium-restricted rats. The maximum effect (-30/-37%) was observed with a dose of 20 micrograms.kg-1. The interruption of the renin-angiotensin system (RAS), obtained by a 7-day infusion of captopril and maintenance doses of angiotensin II, did not cause significant changes in PAC in animals kept on a normal diet, while it did induce a significant lowering of PAC in sodium-restricted rats (-25%). This treatment evoked in both groups of animals a notable reduction of PRA (-61/-89%). A 7-day infusion with ANF (at a rate of 20 micrograms.kg-1.h-1) notably lowered PAC (-32%) in normally-fed rats, independently of the RAS status. The same occurred in sodium-deprived rats, but the effect was more intense in animals with intact RAS (-41% vs -24%). Prolonged ANF infusion significantly reduced PRA (-48%) only in sodium-restricted rats with intact RAS. These findings suggest that (i) the long-term inhibitory effect of ANF on aldosterone secretion is due to both the block of renin release and a direct action on the zona glomerulosa; and (ii) the mechanism underlying the adrenoglomerulotrophic effect of sodium restriction involves not only the activation of RAS, but also the suppression of ANF release.

Animals↗
PubMedDate not supplied

The possible involvement of pancreatic polypeptide in the paracrine regulation of human and rat adrenal cortex.

Pancreatic polypeptide (PP) is a member of a family of 36-amino acid brain-gut peptides, including neuropeptide Y (NPY) and polypeptide YY (PYY) and acting through many subtypes of Y receptors belonging to the superfamily of the G protein-coupled receptors. PP was found to increase both glucocorticoid and cyclic-AMP production by dispersed rat and human adrenocortical cells in a concentration-dependent manner. Minimal and maximal effective concentrations were 10(-10) and 10(-8) M, respectively. The glucocorticoid secretagogue effect of 10(-8) M PP was blocked by the protein kinase A (PKA) unhibitor H-89, but not by the ACTH-receptor antagonist corticotropin-inhibiting peptide (CIP) Autoradiography showed the presence of [125I]PP binding sites in the inner zones of rat and human adrenal cortex, which were not displaced by NPY, PYY, ACTH or CIP. Sizable amounts of PP-immunoreactivity were detected in the medulla of both rat and human adrenals (about 50-100 fmol/mg); this content may give rise, upon submaximal stimulation of PP release, to local intraadrenal concentrations of about 10(-8)/10(-7) M. Collectively, these findings allow us to draw the following conclusions: (i) PP stimulates glucocorticoid secretion, acting through specific receptors coupled with the adenylate cyclase/PKA-dependent signaling pathway; and (ii) PP could be included in that group of regulatory peptides, contained in adrenal medulla, which are able to control the secretory function of the cortex acting in a paracrine manner.

Adrenal Cortex↗
PubMedDate not supplied

Evidence that endogenous somatostatin (SRIF) exerts a tonic inhibitory effect on the rat renin--angiotensin--aldosterone system.

The bolus ip. administration of a SRIF antagonist (SRIF-A) (60 nM/rat) significantly increased renin activity (PRA) and plasma aldosterone concentration (PAC) in rats, without affecting natremia, kalaemia and the blood levels of ACTH or corticosterone. SRIF-A also raised PAC in rats whose renin-angiotensin system had been pharmacologically interrupted by combined captopril/angiotensin-II infusion and in which PRA was very low. The ip. injection of an equimolar dose of SRIF completely reversed these effects of SRIF-A, but the administration of SRIF alone did not affect either PRA or PAC. Taken together, these data would suggest that, in the rat, endogenous SRIF exerts, under basal conditions, a two-fold maximum tonic inhibitory effect on both renin release by kidneys and aldosterone secretion by zona glomerulosa cells.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Long-term trophic action of alpha-melanocyte-stimulating hormone on the zona glomerulosa of dexamethasone -or captopril-treated rats, with or without maintenance doses of ACTH or angiotensin. II: Stereology and plasma hormone concentrations.

The effects of a long-term (7 days) administration of alpha-melanocyte-stimulating hormone (alpha-MSH) on the zona glomerulosa were investigated in "normal" rats and in animals in which the hypothalamic-hypophyseal-adrenal axis and the renin-angiotensin system had been pharmacologically interrupted. alpha-MSH caused a notable hypertrophy of the zona glomerulosa and its parenchymal cells, as well as a significant increase in the plasma concentration of aldosterone, in rats infused with dexamethasone, dexamethasone plus ACTH or captopril plus angiotensin II, but not in animals treated with captopril alone. These findings indicate that alpha-MSH is directly involved in the stimulation of the growth and steroidogenic capacity of rat zona glomerulosa, and that this action of alpha-MSH requires a normal level of circulating angiotensin II.

Adrenocorticotropic Hormone↗