Mazzochi G, Malendowicz L K, Meneghelli V, Gottardo G, Nussdorfer G G
Department of Anatomy, University of Padua, Italy.
Histol Histopathol. 1995 Apr;10(2):359-70.
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.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 chromaffin 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 alpha-helical-CRH and corticotropin-inhibiting peptide (two competitive inhibitors of CRH and ACTH, respectively), but not by 1-alprenolol (a beta-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 well as their basal and maximally angiotensin-II-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 administration of AVP-A1 annulled all these effects of AVP. When infused alone, AVP-A1 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 CRH/ACTH system; however, the physiological relevance of this effect of AVP appears to be doubtful.
精氨酸加压素（AVP）显著增加了分散的球状带（ZG）细胞的基础醛固酮（ALDO）分泌，其作用可被V1受体拮抗剂（AVP-A1）选择性逆转。分散的束状带（ZF）细胞的皮质酮（B）生成不受影响。在正常大鼠中，腹腔内（i.p.）推注AVP可急性提高血浆中ALDO和B的浓度，但在双侧肾上腺切除并带有再生肾上腺皮质自体移植（无髓质嗜铬细胞）的动物中，仅提高了ALDO的血浆浓度。因此，AVP增加了肾上腺切片（包括皮质和髓质组织）的ALDO和B分泌，而仅增加了自体移植组织块的ALDO生成。肾上腺切片对AVP的B反应被α-螺旋促肾上腺皮质激素释放激素（CRH）和促肾上腺皮质激素抑制肽（分别为CRH和促肾上腺皮质激素的两种竞争性抑制剂）阻断，但未被1-阿普洛尔（一种β-肾上腺素能受体拮抗剂）阻断；ALDO反应不受这些拮抗剂中任何一种的影响。连续7天腹腔内输注AVP增加了自体移植组织中ZG细胞和类ZG细胞的体积，以及它们的基础和最大血管紧张素-II刺激的ALDO分泌能力；它还增加了ZF细胞的体积以及基础和最大促肾上腺皮质激素刺激的B分泌能力，但不影响自体移植组织中的类ZF细胞。同时给予AVP-A1可消除AVP的所有这些作用。单独输注时，AVP-A1导致ZG细胞明显萎缩，同时其类固醇生成能力净下降；然而，输注AVP-A1并未改变ZF细胞或自体移植组织中的类ZG和类ZF细胞的形态和功能。综上所述，我们的研究结果使我们能够得出以下结论：（i）AVP在维持和刺激大鼠ZG生长及盐皮质激素分泌活性方面发挥重要生理作用，内源性AVP发挥肾上腺球状带促生长作用可能的来源是肾上腺嗜铬细胞；（ii）AVP通过激活髓质内CRH/促肾上腺皮质激素系统间接刺激大鼠ZF细胞的生长和糖皮质激素分泌活性；然而，AVP这一作用的生理相关性似乎值得怀疑。
