1,721,070 research outputs found
PANCREATIC-POLYPEPTIDE STIMULATES CORTICOSTERONE SECRETION BY ISOLATED RAT ADRENOCORTICAL-CELLS
No full textPancreatic polypeptide (PP) dose-dependently enhanced both basal and submaximally ACTH-stimulated corticosterone production by dispersed zona fasciculata/reticularis cells of the rat adrenal gland. Conversely PP did not affect either basal or ACTH- and angiotensin-II-stimulated aldosterone and corticosterone secretion of zona glomerulosa cells. These findings could throw light on the physiological significance of the marked increase in the pancreatic release of PP during stresses
Galanin in the regulation of the hypothalamic-pituitary-adrenal axis (Review)
No full textGalanin is a regulatory 30- or 29-amino acid peptide, widely distributed in the nervous system and gut, that acts via three subtypes of G protein-coupled receptors, named GAL-R1, GAL-R2 and GAL-R3. Findings have been accumulated that galanin regulates neuroendocrine hypothalamic axes, including the hypothalamic-pituitary-adrenal (HPA) one. Galanin and its receptors are expressed in the hypothalamic paraventricular and supraoptic nuclei, anterior pituitary and adrenal medulla. Adrenal cortex does not express galanin, but is provided with GAL-R1 and GAL-R2. The bulk of evidence indicates that galanin stimulates the activity of the central branch of the HPA axis (i.e. the release of corticotropin-releasing hormone and ACTH), thereby enhancing glucocorticoid secretion from the adrenal cortex. Investigations carried out in the rat show that galanin is also able to directly stimulate corticosterone (glucocorticoid) secretion from adrenocortical cells, through GAL-R1 and GAL-R2 coupled to the adenylate cyclase-protein kinase A signaling cascade, and nor-epinephrine release from adrenal medulla. There is indication that galanin may also enhance corticosterone release via an indirect paracrine mechanism involving the local release of catecholamines, which in turn activate beta-adrenoceptors located on adrenocortical cells. The physiological relevance in the rat of the glucocorticoid secretagogue action of galanin is suggested by the demonstration that the blockade of galanin system significantly lowers basal corticosterone secretion. There is also evidence that galanin plays a role in the modulation of HPA-axis response to stress, as well as in the pathogenesis of pituitary adenomas and perhaps of pheochromocytomas
Acute effects of orexins A and B on the rat pituitary-adrenocortical axis
No full textOrexins A and B are hypothalamic peptides, which act through two receptor subtypes, called OX1R and OX2R. They belong to a group of neuropeptides involved in the central regulation of food intake, members of which (neuropeptide Y and leptin) are known to modulate the function of the pituitary-adrenocortical axis (PAA). We examined the effects at 60 and 120 min of a subcutaneous injection of 5 or 10 nmol/kg of orexins on the function of the rat PAA. Orexin-A raised plasma concentrations of ACTH, aldosterone and corticosterone at both 60 and 120 min, corticosterone response being the most intense one. Orexin-B evoked a sizeable decrease in the plasma level of ACTH, without changing that of corticosterone. The effect of orexin-B on aldosterone plasma concentration was biphasic, the lower dose decreasing and the higher one increasing it at both 60 and 120 min. Evidence indicates that OX1R binds both orexins, while OX2R is selective for orexin-B, and that only OX2R is present in the hypothalamic nucleus paraventricularis. On these grounds, our findings allow us to conclude: (i) OX1R stimulates and OX2R inhibits rat PAA; (ii) orexin-A stimulates PAA, the activation of OX1R prevailing over that of OX2R, while orexin-B suppresses PAA function; and (iii) the aldosterone-secreting response to the higher dose of orexin-B may probably be ascribed to the activation of one or more extra-PAA mechanisms enhancing secretory activity of the zona glomerulosa
Up-regulation of adrenomedullin receptor gene expression in activated local stem cells during rat adrenal regeneration.
No full textPrevious studies showed that adrenomedullin (AM) gene expression was up-regulated in the regenerating rat adrenal cortex after enucleation and contra-lateral adrenalectomy, the effect being significant at day 1 after surgery and peaking between days 3 and 7. Using the same experimental model, we investigated by real time-polymerase chain reaction the mRNA expression of the AM receptor components: calcitonin receptor-like receptor (CRLR) and receptor activity-modifying proteins (RAMP)2 and 3. At time 0 (60 min after enucleation; control group), the CRLR mRNA content was approximately 2- and 5-fold higher than that of RAMP2 and RAMP3, respectively. No significant changes in CRLR mRNA expression were observed in relation to the time elapsed from enucleation. RAMP2 and RAMP3 mRNAs did not exhibit significant changes at day 1 after surgery, but underwent a marked increase between days 3 and 7. The mRNA content of the two RAMPs decreased at days 14 and 28, although remaining significantly higher than that of the controls. These findings indicate that the AM receptor subtypes AM1-R (CRLR-RAMP2) and AM2-R (CRLR-RAMP3) are up-regulated in enucleated adrenals, and the hypothesis is advanced that this effect depends on the increased local production of AM. The concerted increase in AM and its receptor expression would greatly improve the autocrine-paracrine mechanism(s) by which AM favors proliferation of zona glomerulosa stem cells during adrenal regeneration
Neuropeptide Y and glucocorticoid secretion from guinea pig adrenal gland: An in vivo and in vitro study
No full textThe effects of neuropeptide Y (NPY) on adrenal glucocorticoid secretion are controversial, and we have investigated this issue in guinea pigs, where, like in humans and cows, the main glucocorticoid hormone is cortisol. In vivo experiments showed that prolonged NPY administration markedly lowered cortisol plasma concentration not only in normal guinea pigs, but also in animals whose hypothalamic-pituitary-adrenal axis and renin-angiotensin system had been pharmacologically interrupted by the simultaneous administration of dexamethasone and captopril. In vitro experiments ruled out the possibility that in vivo glucocorticoid anti-secretagogue action of NPY can ensue from a direct effect on the adrenal gland. In fact, NPY did not affect cortisol secretion from dispersed guinea pig inner adrenocortical cells. In contrast, NPY raised cortisol production from adrenal slices containing medullary tissue, and this effect was blocked by the beta-adrenoceptor antagonist l-alprenolol. This finding, coupled with the demonstration that NPY enhanced catecholamine release from guinea pigadrenomedullary tissue, strongly suggests that NPY may stimulate glucocorticoid secretion in this species through an indirect mechanism involving catecholamines, that in a paracrine manner promote the secretion of inner adrenocortical cells. In light of these observations, the conclusion is drawn that the in vivo effects of NPY are mediated by mechanism(s) independent of either the suppression of the main adrenal agonists ACTH and angiotensin-II or the direct inhibition of adrenal secretion. The possibility merits an investigation into whether NPY enhances the production of peptides, which, like leptin, inhibit adrenal glucocorticoid secretion acting as circulating hormones
INVESTIGATIONS ON THE ACUTE EFFECTS OF NEUROPEPTIDES ON THE PITUITARY-ADRENOCORTICAL FUNCTION IN NORMAL AND COLD-STRESSED RATS .2. NEUROTENSIN AND NEUROMEDIN-N
No full textThe effects of a subcutaneous bolus injection of 2 micrograms neurotensin (NT) or neuromedin N (NMN) on the function of the hypothalamo-pituitary-adrenocortical axis were investigated in both normal and cold-stressed rats. The blood concentrations of ACTH, corticosterone (B) and aldosterone (ALDO) were measured by specific radioimmunoassays 1, 2 or 4 h after the neuropeptide administration. Cold stress enhanced plasma levels of ACTH, B and ALDO, and these rises lasted unchanged until 4 h. NT did not affect either basal or stress-stimulated plasma levels of ACTH and B, while it lowered the plasma ALDO concentration at 4 h in normal rats and increased it at 1 h in stressed animals. NMN did not change the basal plasma level of ACTH, but it did markedly raise blood levels of both B and ALDO; on the other hand, in cold-stressed rats NMN strongly depressed ACTH response and decreased B plasma concentration at 2 h, without evoking apparent changes in ALDO response. In light of these findings the following conclusions and hypotheses can be drawn and suggested: (i) NT and NMN, when administered at a relatively high dose, do not affect ACTH release in rats under basal conditions; (ii) NMN, but not NT, is able to prevent cold stress-induced stimulation of ACTH secretion, probably by inhibiting hypothalamic thermoregulatory centers; and (iii) NT and NMN exert direct adrenocortical antisecretagogue and secretagogue effects, respectively, which could explain the evident lack of correlation between the levels of circulating ACTH and the plasma concentrations of the main adrenal steroid hormones in both normal and stressed rats after neuropeptide administration
The AT2 receptor-mediated stimulation of adrenal catecholamine release may potentiate the AT1 receptor-mediated aldosterone secretagogue action of angiotensin-II in rats
No full textADRENAL-MEDULLA IS INVOLVED IN THE ALDOSTERONE SECRETAGOGUE EFFECT OF SUBSTANCE-P
No full textSubstance P (SP) increased aldosterone secretion of rat adrenal slices, but not of isolated zona glomerulosa cells, and this effect was annulled by two specific antagonist of SP (SP-A). Both tissue preparations displayed an aldosterone secretory response to isoprenaline (IP) that was blocked by l-alprenolol (AL). AL reversed the aldosterone response of adrenal slices to IP, SP, or IP plus SP, whereas SP-A only suppressed that to SP. Quarters of adrenocortical autotransplants, which are completely deprived of chromaffin cells, showed an aldosterone response to IP, but not to SP. These findings suggest that the mechanism underlying the aldosterone secretagogue action of SP probably involves the stimulation of catecholamine release by adrenal medulla chromaffin cells
Pancreatic polypeptide stimulates rat adrenal glucocorticoid secretion by activating the adenylate cyclase-dependent signaling pathway
No full textEndogenous adrenomedullin system regulates the growth of rat adrenocortical cells cultured in vitro
No full textThe expression of adrenomedullin (AM) system (AM and its receptors), as mRNA and protein, has been detected in the mammalian adrenal zona glomerulosa (ZG) cells. Evidence has been also provided that exogenous AM is able to enhance in vivo and in vitro the proliferative activity of ZG cells. However, the possibility that endogenous AM system may act as a physiological ZG growth regulator has not yet been demonstrated. Hence, we investigated whether the prolonged (48-72 h) suppression of AM gene transcription by a specific antisense oligonucleotide or the long-lasting (24-96 h) blockade of AM receptors by the selective antagonist AM(22-52) are able to affect the growth of rat ZG cells cultured in vitro. Freshly dispersed cells were incubated for 3 h with an AM antisense or a scrambled oligonucleotide, then they were cultured for 48 or 72 h, and proAM mRNA expression and AM content was checked by reverse transcription-polymerase chain reaction and radioimmune assay, respectively. Other ZG cells were cultured in the presence of AM and/or AM(22-52). Growth assay showed that AM (10(-8) M) decreased and AM(22-52) (10(-6) M) increased the duplication time of cultured cells. AM (10(-8) M) raised proliferation index and decreased apoptotic index of cultured cells, and AM(22-52) reversed these effects. AM(22-52) (from 10(-7) to 10(-6) M) and pAM gene suppression by the antisense oligonucleotide significantly lowered proliferation index and increased apoptotic index of cultured cells, both these effects being abrogated by AM (10(-8) M). It is concluded that endogenous AM system plays a relevant role in the autocrine-paracrine regulation of cultured rat ZG-cell growth
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