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Biomedical subjects

J Kolanowski

Publications and source records attributed to J Kolanowski.

At least 73 records · Page 4Linked to original sources
PubMed1975

Potentiation of adrenocortical response upon intermittent stimulation with corticotropin in normal subjects.

Modifications of adrenocortical steroidogenic response to ACTH as a consequence of acute prior exposure to this hormone, were studied in 106 normal subjects divided in 15 experimental groups. Adrenocortical response was assessed by the changes in plasma cortisol level and in urinary excretion of cortisol, 17-ketogenic and 17-ketosteroids; in some experiments plasma 11-deoxycortisol, corticosterone, progesterone and 17-hydroxyprogesterone were determined as well, together with urinary excretion of the unconjugated form of 11-deoxycortisol and corticosterone. Slow (8-h) intravenous administration of ACTH in amounts producing maximal response, leaves the adrenal cortex in a hyperresponsive state in case of further stimulation for up to 3 days, while the adrenocortical secretion comes back to baseline in the meantime. This potentiation phenomenon seems to concern essentially cortisol secretion since, among the compounds measured only cortisol and 11-deoxycortisol secretions increased progressively in amplitude when ACTH was administered repeatedly. Futhermore the degree of ACTH-induced adrenocortical hyperresponsiveness was found to depend on the amount of ACTH injected and on the time during which the adrenal cells are exposed to high peptide hormone concentrations. Increased adrenocortical responsiveness to ACTH persists when endogenous corticotropin secretion was suppressed for a few days by dexamethasone in normal subjects. Thus the potentiation phenomenon is not critically dependent on continued exposure of adrenal cells to endogenous corticotropin.

Adrenal Cortex↗
PubMed1973

Rate of uptake of endogenous cortisol by the left ventricle of the anaesthetized dog during ventilation with ambient air and during hypoxia.

1. The rate of uptake of endogenous cortisol by the left ventricle was determined in eight dogs as the product of the left ventricular myocardial plasma flow and the coronary arteriovenous difference in plasma cortisol concentration. The arteriovenous difference in hormone concentration in resting skeletal muscle (M. gracilis) was also measured. The values given are means +/- S.E.2. During ventilation with ambient air (arterial P(O2): 85 +/- 2 mm Hg), the rate of cortisol uptake by the left ventricle averaged 382 +/- 92 ng/100 g.min. The arteriovenous difference in hormone concentration in the vessels of the M. gracilis was more than twice that in the coronary vessels. Assuming a value of 3-4 ml./100 g.min for the blood flow in this muscle, the corresponding rate of cortisol uptake would be in the range of 25-33 ng/100 g.min.3. During hypoxia (arterial P(O2): 35 +/- 1 mm Hg), the rate of cortisol uptake by the left ventricle was not significant, averaging 26 +/- 113 ng/100 g.min. By contrast, the skeletal muscle still extracted significant amounts of cortisol from the plasma. It is inferred that the suppression of a significant uptake of the hormone by the left ventricle was related, at least in part, to the changes in the mechanical and associated metabolic activity of the heart muscle elicited by the lowering of the arterial P(O2).4. Hypoxia depressed the net uptake of cortisol by the left ventricle rather than the uptake mechanism itself. Indeed, bi-directional movements of cortisol between the plasma and the heart muscle, with rates of release up to 1150 ng/100 g.min, were observed.

Air↗
PubMedDate not supplied

Characteristics of the response of human adrenocortical cells to ACTH.

The effects of adrenocorticotrophic hormone (ACTH) on human adrenocortical steroidogenesis were studied in adrenocortical cells which had been isolated from normal and hyperplastic glands by a technique combining tyrpsin digestion and mechanical dispersion, and incubated in the presence of ACTH or dibutyryl cyclic AMP (dbcAMP). The response was measured in terms of cyclic AMP, cortisol, corticosterone, 11-deoxycortisol and cortisone production. A classical sigmoid curve, calculated by non-linear, least square method, related the increase in cAMP production or in steroidogenesis to the log dose of ACTH. For the normal adrenocortical cells, the estimated concentration of ACTH inducing a half-maximal response was approximated 2h0 pg ACTH 1-24/ml for steroidogenesis, against 437 pg/ml for cAMP production. The estimated Vmax (per 107 cells/ml, on average) was 27 pmol cAMP/2 and for steroidogenesis (in ng/2 h): 188 for cortisol, 106 for corticosterone, 37 for 11-deoxycortisol, and 32 for cortisone, dbcAMP (1.0 mM) stimulated steroidogenesis to a comparable extent. The cells from a hyperplastic adrenal gland exhibited a steroidogenic response to ACTH and dbcAMP which was 2-3 times greater than the response of a similar number of normal adrenocortical cells. Calculated per pmol cAMP generated, the ACTH-stimulated cortisol production by cells from hyperplastic gland was also increased with respect to normal cell response. These data suggest a prolonged effect of ACTH on cortisol biosynthetic pathway beyond the membrane step of cAMP generation.

Adrenal Cortex↗