Production of Steroids by in Vitro Superfusion of Endocrine Tissue. II. Steroid Output from Bisected Whole, Capsular and Decapsulated Adrenals of Normal Intact, Hypophysectomized and Hypophysectomized-Nephrectomized Rats as a Function of Time of Superfusion

Abstract

Steroid output from adrenals of normal intact rats and rats 3 hr and 2 days after hypophysectomy has been measured during continuous superfusion in vitro (1, 2). Comparison of outputs from bisected whole glands, capsular (fibrous capsule plus mainly zona glomerulosa) and decapsulated (mainly zona fasciculata-reticularis plus medulla) tissue has shown that 3 of the 4 steroids examined, 18-hydroxy-β4, 18-hydroxy-DOC and corticosterone, were produced to some extent by both zones of the adrenal cortex but aldosterone production was restricted to the zona glomerulosa under all conditions studied. A reproducible decline in steroid output with time of superfusion was observed for all 3 types of tissue taken from normal intact rats. Three and 48 hr after hypophysectomy the production of the 3 steroids by the zona fasciculata was lowered and the decay virtually abolished. A continuous infusion of ACTH (60 mU/ml medium) maintained steroid output from the zona fasciculata of intact rats at the high initial level for the first 3 hr of superfusion and rapidly increased the output from glands of acutely hypophysectomized rats to about the same level. However, a slow decline in output was still observed, particularly at the later time intervals. Neither hypophysectomy nor hypophysectomy plus nephrectomy markedly affected steroid output from the zona glomerulosa either as regards μg produced or the shape of the decay curves but the rate of decline in steroid output with time was decreased following sham nephrectomy. A continuous infusion of ACTH increased the initial output of all 4 steroids 2- to 3-fold; the outputs then declined at a rate some 5-fold greater than that observed with zona fasciculata tissue. A continuous infusion of a high dose of angiotensin II (2.8 μg/ml medium, 116 μg/hr) also failed to markedly increase steroid output from zona glomerulosa tissue of hypophysectomized-nephrectomized rats. Possible reasons for the decay in steroid output have been examined and it is suggested that one explanation is the decay in vitro of the stimulus to steroid secretion operating in vivo1. (Endocrinology86: 360, 1970)