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At least 559 records · Page 31Linked to original sources
PubMed1978

[Changes in the adrenal cortex during adaptation to different regimes of motor activity].

The hypertrophy of the adrenal glands was higher in the rats adapted to long-lasting exercises of moderate and mild intensities. Ultrastructural analysis showed that there were more mitochondria and vesicular cristae as well as the elements of cytoplasmatic reticulum and lipid droplets in the cells of adrenal cortex of the adapted rats. The data obtained suggest two types of adaptational changes in the adrenal cortex: 1) pronounced hypertrophy with low spontaneous functional activity and increased content of cytochrome a--a3; 2) less pronounced hypertrophy with higher content of corticosterone and lower content of cytochrome a--a3 in adrenals.

Adaptation, Physiological↗
PubMed1995

Effects of oxytocin on the function and morphology of the rat adrenal cortex: in vitro and in vivo investigations.

The effects of oxytocin (OX) on the function and morphology of the rat adrenal cortex were studied in vivo and in vitro. OX exerted a potent stimulatory action on basal, but not 10(-8) M ACTH-stimulated corticosterone (B) secretion of dispersed rat inner (zona fasciculata and zona reticularis) adrenocortical cells (maximal effective concentration: 10(-9) M); in contrast, at higher concentrations (10(-7)/10(-6) M) OX inhibited maximally ACTH-stimulated B output. A single subcutaneous (s.c.) injection of 1.2 nmol/100 g body weight OX resulted in a long-lasting (up to 12 h) rise in plasma B concentration (PBC). The prolonged administration of OX (daily s.c. injections of 0.6 or 1.2 nmol/100 g for 10 days) caused a marked lowering in the adrenal weight and volume of all adrenocortical zones, that in turn was due to a decrease in the number of their parenchymal cells; however, the average volume of inner adrenocortical cells was significantly increased. Basal PBC was lowered, but its response to ether stress was unchanged in comparison with control rats. Prolonged OX treatment did not change B secretion by adrenal slices, but it markedly raised that of dispersed inner adrenocortical cells. Our present findings clearly show that the effects of OX on the adrenal cortex depend on the experimental model employed (in vitro versus in vivo) and the duration of treatment (acute versus chronic). Taken together they allow us to conclude that OX exerts an acute direct stimulatory effect on the rat adrenal cortex, and a chronic inhibitory one, that at least in part could be due to the interference of OX with the mechanism(s) of intracellular transduction of the ACTH secretagogue signal.

Adrenal Cortex↗
PubMed1982

Effect of thyroidectomy on the rat adrenal cortex enzyme activities involved in corticosterone and aldosterone biosynthesis.

The effect of thyroidectomy on corticosterone and aldosterone biosynthesis, in rat adrenal cortex, were investigated in vitro. Thyroidectomy slowed down by about 30% the activity of microsomal 21 hydroxylase and mitochondrial 11 beta hydroxylase, the two stages leading to corticosterone formation from progesterone. The plasma corticosterone concentration also diminished in thyroidectomized rat. The mitochondrial enzyme system catalyzing the conversion of corticosterone into aldosterone included both 18 hydroxylase and 180H dehydrogenase. In the absence of thyroid hormone, values of both enzyme activity slowed down by about 30%. Thus thyroidectomy induced a general decrease in all mitochondrial hydroxylation processes requiring NNADPH as energetic cofactor. Mitochondrial NADPH was mainly synthesized by the activity of NADP+ malic enzyme and pyridine nucleotide transhydrogenase; the activity of both enzymes was determined in submitochondrial particles from adrenal cortex of normal and thyroidectomized rats. The activity of NADP+ malic enzyme and non energy-dependent transhydrogenase in the direction of NADPH formation dropped significantly after thyroidectomy, thus reducing the amount of NADPH available for hydroxylating mechanisms. The results should be compared to the large rise in th cytosolic malic enzyme level caused by thyroidectomy. The latter also ensured that the transhydrogenase reaction did not vary in the direction of NADP+ formation. Further, the drop in NADPH synthesis after thyroidectomy was coupled with a decrease in phosphorylation rate of added ADPH by adrenal cortex mitochondria of thyroidectomized rat. These findings might account for the general decline in the energy-dependent processes involved in steroidogenesis, a decline mainly due to the lowering of the H+ ions gradient driving ATP and NADPH synthesis through electron transfer.

Adrenal Cortex↗