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Biomedical subjects

E Stark

Publications and source records attributed to E Stark.

At least 127 records · Page 7Linked to original sources
PubMed1975

Effect of intraventricular glutamate on ACTH release.

Sodium glutamate infused into the 3rd ventricle is a potent stimulus of ACTH release, as shown by the rise in plasma corticosterone levels. Glutamate failed to consistently increase the plasma corticosterone level in rats with deafferentation of the medial basal hypothalamus (MBH). We suggest that intraventricular glutamate interferes with central nervous function outside the MBH and stimulates ACTH release via afferent neural pathways.

Adrenocorticotropic Hormone↗
PubMed1975

Adrenal potassium and sodium in experimental hyper- and hypoaldosteronism in the rat. Determination by electron probe x-ray microanalysis.

Potassium and sodium contents in the various adrenal zones were determined in experimental hyper- and hypoaldosteronism in the rat by electron probe X-ray microanalysis. The analysis aimed at revealing intracellular values. There was no change in the potassium content of the zona glomerulosa, zona fasciculata and medulla neither in hyperaldosteronism induced by Na-deficiency, nor in hypoaldosteronism, elicited by Na-rich diet. The sodium content in the zona glomerulosa and zona fascicularis was increased in the Na-loaded rats, while that of the medulla was not changed. Our data are not consistent with the hypothesis that a change of adrenal intracellular potassium would act as a final stimulus in the regulation of aldosterone secretion.

Adrenal Glands↗
PubMed1975

Corticosteroid receptors in the central nervous system of the rat.

Corticosteroid receptors were demonstrated in the medial hypothalamus, the hippocampus and the parietal cortex of the rat while no such receptors were found in the hypophysis, the amygdala and the anterior hypothalamus. The findings suggest the role of extrahypothalamic regions in the perception of corticosteroid feedback as well as in the regulation of the hypothalamo-hypophysial-adrenal function and do not support the assumption that corticosteroids would inhibit corticotrophin secretion by acting directly on the hypophysis.

Adrenal Glands↗
PubMed1975

[Ultrastructure and hormone secretion of a tissue culture from an adrenal gland tumor simulating Cushing's syndrome].

Tissue cultures of a surgically removed adrenocortical tumour causing Cushing's syndrome, and tissue cultures from the attached, tumour-free adrenal were studied. There were two cell types characteristic of tumour tissue. The cell type occurring most frequently had pronounced hypertrophied agranular endoplasmic reticulum. A fewer number of lipidrich cells containing many electron-dense granules could also be found. The ratio of cells changed during cultivation. In the 17 days tumour culture, a higher percentage of lipid-rich cells could be observed. In spite of continuous ACTH treatment, the initially high hydrocortisone level decreased, gradually. It may be assumed that the lipid-rich cells are of reduced ability as regards hydrocortisone production.

Adrenal Cortex↗
PubMed1975

Role of prostaglandin E2 in the stimulatory effect of ACTH on ovarian blood flow.

It has been studied in dogs anaesthetized with chloralose-urethane whether Prostaglandin E2(PGE2) might act as a mediator of the stimulatory effect of ACTH on ovarian blood flow. Without any damage to the ovarian vessels, a heated thermocouple was inserted into the stroma of the ovaries and local blood flow was recorded continuously. Similarly to ACTH, PGE2 (100 ng/kg/min) infused into the ovarian bursa increased local blood flow. The ovaries were isolated in situ and perfused by a peristaltic pump from the femoral artery. Synthetic ACTH or PGE2 was infused into the ovarian artery for 15 min and perfusion pressure was measured. Both ACTH (12.5--25.0--50.0--100.0 ng/kg/min) and PGE2 (3912--6.25--12.50--25.00 ng/kg/min) reduced perfusion pressure, caused vasodilatation. There was a significant linear correlation between the degree of vasodilatation and the logarithm of the doses. If the doses of the two agents are expressed in terms of mols, the effect of both agents can be characterized by a common equation. Fifty--200 mug/kg indomethacin inhibited the effect of ACTH but increased the effect of PGE2. It is suggested that in dogs ACTH exerts its ovarian blood flow stimulatory effect by releasing PGE2 or some similar agent(s).

Adrenocorticotropic Hormone↗
PubMed1975

Stress-induced ACTH release after removal of the hypothalamus in rats with atrophied neural lobe.

Twenty-four hours after isolation of the pituitary by surgical removal of the medial hypothalamus, i.e. in rats with pituitary island, E. coli endotoxin significantly increased the plasma corticosterone level. Atrophy of the neural lobe, due to pituitary stalk section performed one month prior to removal of the medial hypothalamus, did not prevent the increase of ACTH release by E. coli endotoxin. E. coli endotoxin-induced ACTH release in MBH-deprived animals does not appear to be a function of mechanisms operating only in the innervated lobe.

Adrenocorticotropic Hormone↗