Abstract
An electron microscopical observation was made on the adrenal cortex of rats under hyper-and hypofunctional experiments. Such stimulative factors as administration of ACTH, unilateral adrenalectomy and injection of snake toxin were noted to commonly dilate the anastomosing tubules of the agranular endoplasmic reticula (ER) in the fasciculata cells throughout their length. Furthermore these factors diminished quickly the number of fat droplets. On the other hand, prevention of the pituitary ACTH release due to hypophysectomy induced retrogression of the tubular ER, storage of the fat droplet and destruction of the mitochondria in the atrophic fasciculata cells. The osmiophilic substance was deposited initially in the confluences of anastomosing tubular ER and grew thereafter into the fat droplet. The probable reason for the rapid loss of fat droplets from the stimulated cells is that the content of fat droplets is transported through the tubular ER. However, in deficiency of the circulating ACTH, fat droplets were stabilized without movement on account of atrophy of the ER. In fact, they increased in number and in size. Elevated ACTH levels resulted in an approximation of the ER to the mitochondria, and the limiting membrane of ER was often adhesive to the external membrane of mitochondria. This topographic connection is favourable to our views that biosynthesis of steroid hormones would be carried out in the lumen of the anastomosing canalicular ER in participation with the enzymes laden on the membranes of mitochondria and ER. The final product of these duct systems seemed to be discharged into the intercellular space, because there was evidence that the terminals of the tubular ER opened into the intercellular space under hyperfunctional conditions.
