In-vitro and in-vivo studies of the effects of arginine-vasopressin on the secretion and growth of rat adrenal cortex

• Mazzocchi, G. ^[1] ; Malendowicz, L.K. ^[2] ; Meneghelli, V. ^[1] ; Gottardo, Giuseppe ^[1] ; Nussdorfer, G.G. ^[1]
  1. [1] University of Padua

     University of Padua

     Padova, Italia

     
  2. [2] Department of Histology and Embryology, School of Medicine, Poznan, Poland
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 10, Nº. 2, 1995, págs. 359-370
• Idioma: inglés
• Enlaces
  • Texto completo
• Dialnet Métricas: 2 Citas
• Resumen

  • 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.