Short-term ACTH treatment provoked a decrease in volume of the lipid-droplet compartment in rat zona glomerulosa cells, and a rise in plasma and intracellular concentrations of corticosterone and aldosterone. It enhanced activities of 3 beta-hydroxysteroid dehydrogenase (3 beta HSD), 11 beta-hydroxylase (11 beta OH) and 18-hydroxylase (18OH). Long-term ACTH administration produced a hypertrophy of the zona glomerulosa and its parenchymal cells, a result of the increase in volume of the smooth endoplasmic reticulum and the mitochondrial compartment. The surface area per cell of mitochondrial inner membranes increased; the tubular cristae were transformed into a homogeneous population of vesicles. The plasma and intracellular concentrations of corticosterone further increased, whereas those of aldosterone fell below basal levels (the "aldosterone-escape" phenomenon). The activities of 3 beta HSD and 11 beta OH were enhanced, that of 180H decreased. Therefore, ACTH stimulates zona glomerulosa growth and transforms parenchymal elements into zona fasciculata cell-types. Cyanoketone nullified acute ACTH effects on plasma and intracellular concentrations of corticosterone and aldosterone, but did not affect the activities of 11 beta OH and 18OH. Chronic ACTH treatment produced similar results, although 18OH activity was not suppressed. The mechanism underlying the "aldosterone-escape" phenomenon may thus involve a rise in the intracellular concentration of corticosterone, caused by the enhanced synthesis and activation of 3 beta HSD and 11 beta OH.

The effects of Nafenopin, a hypolipidemic drug, on the zona fasciculata of the rat adrenal cortex were investigated by biochemical, stereological, and cytochemical methods. Chronic Nafenopin treatment (5 days) significantly lowered serum cholesterol level, while it did not alter blood corticosterone concentration and 11beta-hydroxylase activity of adrenocortical cells. Stereology showed a significant increase in the average volume of zona fasciculata cells, which was almost exclusively due to smooth endoplasmic reticulum (SER) proliferation. The volume of lipid compartment was significantly reduced, whereas the volume of diaminobenzidine (DAB)-positive bodies (peroxisomes) per cell displayed a marked increase. Cholesterol administration per os to the treated animals raised the serum cholesterol level and completely reversed the Nafenopin effects. One day of Nafenopin administration provoked a slight but significant lipid depletion in adrenocortical cells, while 3 days of continuous drug treatment induced an extreme lipid depletion and a moderate increase in the SER coupled with a significant decrease in the plasma concentration of corticosterone. Since microsomal fraction and catalase seem to be involved in the cholesterol metabolism and utilization, the hypothesis is advanced that the Nafenopin-elicited SER and peroxisome proliferation is a compensatory response enabling adrenocortical cells to maintain an adequate level of hormonal output.

The effects of a chronic treatment with ACTH and dexamethasone on the zona glomerulosa of intact rat adrenals were investigated by morphometric methods and electron microscopy. It was found that ACTH increases the volume of the zona glomerulosa, of the cells, nuclei, mitochondrial compartment as well as the surface of SER and mitochondrial cristae. Also noticeable was the hypertrophy of the Golgi apparatus. Opposite effects were obtained after dexamethasone treatment. These findings are interpreted as indicating that ACTH is involved in the maintenance and stimulation of the growth and steroidogenic capacity of the adrenal zona glomerulosa.Numerous lines of evidence suggest that ACTH stimulates aldosterone secretion by the zona glomerulosa (Müller 1971); however, a role of ACTH in the maintenance and stimulation of the growth and steroidogenic capacity of this zona has not yet been clearly established.In previous investigations we found that 11 days after hypophysectomy there is conspicuous atrophy of the zona glomerulosa in rat adrenals, and that chronic treatment for 6 consecutive days with ACTH reverses this effect of hypo¬ physectomy (Nussdorfer et al. 1973). Recently, Nickerson 8c Brownie (1975) confirmed the atrophy of the zona glomerulosa 7 days after hypophysectomy, but found the volume of the zona restored to the control value at the 30th day after operation.

The effects of \g=a\-melanocyte-stimulating hormone (\g=a\-MSH) on the rat adrenal cortex were investigated by coupled morphometric and radioimmunological techniques. Short-term \g=a\-MSHadministration provoked a significant increase in the aldosterone plasma level along with a notable lipid droplet depletion in zona glomerulosa cells. Long-term \g=a\-MSHtreatment induced a notable hypertrophy of zona glomerulosa cells and a further rise in the blood concentration of aldosterone. \g=a\-MSHdid not affect zona fasciculata morphology and corticosterone plasma level. The possibility is discussed that \g=a\-MSHmay be specifically involved in the control of the growth and steroidogenic capacity of rat adrenal zona glomerulosa.Many lines of evidence indicate that cc-melanocyte-stimulating hormone (ct-MSH) is a power¬ ful stimulator of aldosterone output by rat zona glomerulosa cells in vitro (Vinson et al. 1980(Vinson et al. , 1981aSzalay & Stark 1982; Hinson et al. 1985; Jornot et al. 1985), and that zona glomerulosa cells possess high-affinity receptors for ct-MSH (Vinson et al. 1983(Vinson et al. , 1984. In vivo effects of ct-MSH on the adrenal cortex were object of sparse investigations (Sugihara et al. 1982;Shenker et al. 1985). It therefore seemed worthwhile to study, by coupled morphometric and radioimmunological techniques, the effects of shortand long-term a-MSH administration on the rat adrenal cortex.

Abstract. The effects of short and prolonged treatments with prolactin on the morphology and hormone secretion of the rat adrenal zona glomerulosa were investigated by coupled morphometric and radioimmunological techniques. Short-term prolactin administration did not alter plasma aldosterone concentration or zona glomerulosa morphology. Conversely, chronic prolactin treatment caused both a notable hypertrophy of zona glomerulosa cells and a significant rise in the blood level of aldosterone. The possibility is discussed that prolactin may be involved in the control of the growth and steroidogenic capacity of the rat adrenal zona glomerulosa.