Browsing by Subject "Adrenal cortex"
Now showing 1 - 9 of 9
Results Per Page
Sort Options
- PublicationOpen AccessAge-dependent changes in the function and morphology of mitochondria of rat adrenal zona fasciculata(Murcia : F. Hernández, 1994) Markowska, A.; Rebuffat, P.; Gottardo, Giuseppe; Mazzocchi, G.; Nussdorfer, G.G.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). Stereology showed a notable age-dependent increase in the number of mitochondria per unit cell-volume, coupled with a marked decrease in their average volume. The width of the mitochondrial intermembrane space remained unchanged, but its average volume strikingly decreased. This last finding fits well with the enhanced capacity of mitochondria to produce PREG, since intermembrane space is an acqueous barrier to the translocation of free cholesterol from the outer membrane to the cristae, where cytochrome-P450scc is located. In conclusion, the hypothesis is advanced that all these age-related functional and morphological mitochondrial changes are an ACTH-dependent compensatory response enabling ZF cells to partially counteract their decreased glucocorticoid secretory capacity, which in turn is due to the impaired utilization of intracytoplasmic stores of cholesterol esters.
- PublicationOpen AccessEffects of bombesin on the morphology and(Murcia : F. Hernández, 1995) Malendowicz, L.K.; Nussdorfer, G.G.; Miskowiak, B.; Majchrzak, M.The acute and chronic effects of bornbesin (BM) on the structure and function of rat adrenal cortex were investigated by rnorphornetric and radioirnrnunological techniques. An intraperitoneal bolus injection of 2 yglrat BM rnarkedly raised plasma corticosterone (B) concentration (PBC). The intraperitoneal BM infusion (1 yg/rat.h-l) for 1, 2 or 4 days evoked a notable increase in the nurnber of adrenocortical cells, without inducing apparent changes in either PBC or B output by adrenal quarters. Since proliferation and expression of specialized functions are rnutually exclusive states of cells, our findings suggest that the conspicuous stirnulation of adrenocortical-cell proliferation evoked by BM infusion may be responsible for the apparent lack of effect of this treatrnent on B secretion.
- PublicationOpen AccessEffects of pneumadin (PNM) on the adrenal glands. 5.Potent stimulating action of PNM on adrenocortical growth of dexamethasone-administered rats(Murcia : F. Hernández, 1996) Markowska, A.; Macchi, C.; Nussdorfer, G.G.; Malendowicz, L.K.Pneumadin (PNM) is a biologically active decapeptide, originally isolated from mammalian lungs, that has been previously found to acutely stimulate pituitary-adrenocortical axis in rats. The effects of 2-day PNM administration on the atrophic adrenal cortices of rats treated for 8 days with dexamethasone (DX) were investigated. PNM significantly raised adrenal weight and the average volume of adrenocortical cells. The decapeptide strikingly increased ACTH plasma concentration; however, the blood levels of aldosterone and corticosterone, as well as steroid output by adrenal quarters were not apparently affected. In light of these findings the following conclusions can be drawn: (i) PNM enhances the growth of adrenal cortex in DXadministered rats by a mechanism involving the stimulation of ACTH release; and (ii) PNM treatment is probably too short to allow DX-atrophied adrenocortical cells to re-acquire al1 their differentiated secretory capacities.
- PublicationOpen AccessEffects of pneumadin (PNM) on the adrenal glands. 6. Further studies on the inhibitory effect of PNM on dexamethasone-induced(Murcia : F. Hernández, 1997) Markowska, A.; Andreis, P.G.; Miskowiak, B.; Nussdorfer, G.G.; Malendowicz, L.K.Pneumadin (PNM) is a biologically active decapeptide, which has previously been found to enhance rat adrenal growth; the mechanism is indirect and probably involves the stimulation of both argininevasopressin (AVP) and ACTH release. The effects of 2- and 6-day PNM administration on the atrophic adrenal cortices of rats treated for 8 and 12 days, respectively, with daily subcutaneous injections of 15 or 40 g1100 g body weight of dexamethasone (Dx) were investigated. Morphometry showed that PNM counteracted Dxinduced adrenal atrophy, by preventing the decrease in volume and number of the parenchymal cells. PNM raised aldosterone and corticosterone production of adrenal quarters from Dx-treated rats, but it did not evoke significant changes in the plasma concentrations of the two hormones. The preventive effect of PNM was only partial and almost exclusively evident in rats administered the lower dose of Dx. In light of these findings the following conclusions are drawn: (i) PNM is able to partially overcome the Dx-induced inhibition of the rat hypothalamo-pituitary-adrenal axis, probably by stimulating the pituitary release of AVP and ACTH, that in turn enhance adrenocortical growth; (ii) the PNMinduced improvement of the secretory capacity of atrophic adrenocortical cells is not sufficient to raise the blood leve1 of corticosteroid hormones; and (iii) Dx exerts a direct inhibitory action on adrenocortical cells, which is not counteracted by PNM.
- PublicationOpen AccessEndothelin-1 [1-311 acts as a selective ETA-receptor agonist in the rat adrenal cortex(Murcia : F. Hernández, 2001) Rebuffat, P.; Malendowicz, L.K.; Neri, G.; Nussdorfer, G.G.Endothelin-1 (ET-1) is a 21-amino acid residue (ET-1[1-211) hypertensive peptide, which together with its receptor subtypes A and B (ETA and ETB) is expressed in the rat adrenal cortex, where it stimulates steroid-hormone (aldosterone and corticosterone) secretion through the ETB receptor and the growth (proliferative activity) of the zona glomerulosa (ZG) through the ETA receptor. ET-1[1-211 is generated from bigET-1 by the endothelin-converting enzyme (ECE-1). However, recent evidence indicates the existence of an alternative chymase-mediated biosynthetic pathway leading to the production of an ET- 1[1-311 peptide, which was found to reproduce the ETA receptor-mediated vascular effects of ET-l[l-211. We found that ET-1[1-211, but not ET-1[1-311, concentration-dependently raised steroid secretion from dispersed rat adrenocortical cells, its effect being blocked by the ETB-receptor selective antagonist BQ- 788. Both ET-1s concentration-dependently increased the number of "S-phase" cells (as detected by the 5- bromo-2'-deoxyuridine immunocytochemical method) in capsule-ZG strips within a 240 min incubation. The ZG proliferogenic action of both ET-1s was blocked by the ETA-receptor antagonist BQ-123, and ET-l[l-311 was found to be significantly more potent than ET-1[1- 211. Autoradiography showed that in the rat adrenal ET- 1[1-211 displaced the binding of selective ligands to both ETA ( [ 1 2 5 ~ ] ~ ~1-21425) and ETB receptors ( [ 1 2 5 ~ ] ~ ~ - 3020), while ET-l[l-311 eliminates only the binding to ETA receptors. Collectively, our findings provide strong evidence that ET-1[1-311 acts in the rat adrenal glands as a selective ETA-receptor agonist, mainly involved in the stimulation of ZG proliferative activity.
- PublicationOpen AccessHistological parameters of the adrenal cortex after testosterone application in a rat model of the andropause(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Ajdžanović, Vladimir Z.; Jarić, Ivana M.; Živanović, Jasmina B.; Filipović, Branko R.; Šošić Jurjević, Branka T.; Ristić, Nataša M.; Stanković, Sanja D.Histological analysis of the adrenal cortex, after testosterone application in a rat model of the andropause, was the main subject of the present study. Middle-aged Wistar rats were divided into shamoperated (SO; n=8), orchidectomized (Orx; n=8) and testosterone treated orchidectomized (Orx+T; n=8) groups. Testosterone propionate (5 mg/kg b.m. /day) was administered for three weeks, while SO and Orx groups received the vehicle alone. Histological objectives were achieved using stereology, histochemistry and steroid receptor immunostaining. The concentrations of testosterone, aldosterone, corticosterone and DHEA were determined by immunoassays. Expectedly, increased (p<0.05) serum concentration of testosterone was observed in Orx+T group. The volume of ZG cells and nuclei increased in Orx+T animals by 50% and 25% (p<0.05) respectively, but the serum concentrations of aldosterone decreased (p<0.05) by 60%, all compared to the same parameters in Orx group. The immunostaining for androgen receptors (ARs) suggested their cytoplasmic localization in ZG cells of Orx+T rats. Volume of the ZF cell nuclei in Orx+T group decreased (p<0.05) by 17%, which was followed by the significant (p<0.05) fall in corticosterone production and secretion, all in comparison with Orx animals. Also, nuclear immunolocalization of ARs of high optical density was observed through the ZF of Orx+T group. In Orx+T rats volume of ZR cells and nuclei, and circulating DHEA concentration increased (p<0.05) by 68%, 22% and about 6.6 times respectively, compared to Orx animals. Besides the extra-receptor actions in adrenal cortex, testosterone supposedly affects some steroidogenesisrelated gene expression, as indicated by centripetal rise in the number of nuclear ARs.
- PublicationOpen AccessIn-vitro and in-vivo studies of the effects of arginine-vasopressin on the secretion and growth of rat adrenal cortex(Murcia : F. Hernández, 1995) Mazzocchi, G.; Malendowicz, L.K.; Meneghelli, V.; Gottardo, Giuseppe; Nussdorfer, G.G.Arginine-vasopressin (AVP) markedly increased basal aldosterone (ALDO) secretion by dispersed zona-glomerulosa (ZG) cells, and its effect was selectively reversed by VI-receptor antagonists (AVP-Al). Corticosterone (B) production by dispersed zona fasciculata (ZF) cells was not affected. The bolus intraperitoneal (i.p.) administration of AVP acutely raised the plasma concentrations of both ALDO and B in normal rats, but only that of ALDO in bilaterally adrenalectomized animals bearing regenerated adrenocortical autotransplants, which are deprived of medullary chromafin cells. Accordingly, AVP raised ALDO and B secretions by adrenal slices (including both cortical and medullary tissues), and only ALDO production by autotransplant quarters. The B response of adrenal slices to AVP was blocked by a-helical-CRH and corticotropin- inhibiting peptide (two competitive inhibitors of CRH and ACTH, respectively), but not by 1-alprenolol (a B-adrenoreceptor antagonist); ALDO response was not affected by any of these antagonists. A 7-day i.p. infusion with AVP increased the volume of ZG cells and ZG-like cells of autotransplants, as weli as their basal and maximally angiotensin-11-stimulated ALDO secretory capacity; it also raised the volume, and basal and maximally ACTH-stimulated B secretory capacity of ZF cells, but it did not affect ZF-like cells of autotransplants. The simultaneous adrninistration of AVP-A1 annulled al1 these effects of AVP. When infused alone, AVP-Al caused a marked atrophy of ZG cells, coupled with a net drop in their steroidogenic capacity; however, AVP-A1 infusion did not change the morphology and function of either ZF cells or ZG-like and ZF-like cells of autotransplants. Taken together, our findings allow us to draw the following conclusions: (i) AVP plays an important physiological role in the maintenance and stimulation of ZG growth and mineralocorticoid secretory activity in rats, the source of endogenous AVP exerting adrenoglomerulotropic action probably being adrenal chromaffin cells; and (ii) AVP indirectly stimulates the growth and glucocorticoid secretory activity of rat ZF cells, by activating intramedullary CRHIACTH system; however, the physiological relevance of this effect of AVP appears to be doubtful.
- PublicationOpen Accesslmmunocytochemical correlates of an extrapituitary adrenocortical regulation in man(Murcia : F. Hernández, 1997) Heym, C.Investigations reviewed in this article provide cytochemical and functional support for a significant involvement of extrapituitary factors in human adrenocortical functions. Among these factors neural messengers may play a crucial role in the adrenocortical regulation, arising from specifically coded postganglionic neurons with both, extrinsic and intrinsic locations, as well as from chemically characteristic afferent neurons. The close association of varicose transmitter segments with steroid hormone synthesizing cells and their occurrence at arteries and sinusoid capillaries are indicative for both direct and indirect regulatory mechanisms on cortical functions. The immunohistochemical presence of neuropeptides and cytokines in endocrine andlor immune cells of the human adrenal medulla and cortex as well as specific binding sites on steroidogenic cells indicate the modulatory implication of additional short-paracrine-and ultrashort-autocrine-feedback loops on cortical cell proliferation and steroid metabolism. The summarized data suggest that basa1 endocrine influence of the hypothalamo-pituitary axis on adrenocortical growth and functions in man is controlled by the nervous system that also regulates local fine-tuning of human cortical activity.
- PublicationOpen AccessProlonged kallikrein inhibition does not affect the basal growth and secretory capacity of rat adrenal cortex, but enhances mineralo- and glucocorticoid response to ACTH and handling stress(Murcia : F. Hernández, 2000) Rebuffat, P.; Neri, G.; Bahgelioglu, M.; Malendowicz, L.K.; Nussdorfer, G.G.The effects on the pituitary-adrenocortical functions of the prolonged (7-day) blockade of endogenous bradykinin (BK) synthesis, obtained by the administration of the kallikrein inhibitor (K-I) cyclohexylacetyl-Phe-Arg-Ser-Val-Gln amide, were investigated in the rat. K-I treatment did not cause significant changes in the (i) body and adrenal weights; (ii) basal plasma levels of ACTH, aldosterone and corticosterone; and (iii) average volume of adrenocortical cells and their basal secretory capacity. Conversely, K-I administration induced a significant magnification of the in vivo mineralo- and glucocorticoid responses to the intraperitoneal (i.p.) bolus injection of ACTH. Moreover, K-I-treated rats, but not control ones, displayed a moderate and short-term adrenal secretory response to the mild stress evoked by the placebo i.p. injection. Collectively, these findings rule out the possibility that endogenous BK plays a relevant role in the control of adrenocortical function under basal conditions. However, they suggest that endogenous BK may be involved in quenching exceedingly high adrenocortical responses to ACTH and stresses.