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PubMed1977

[Effect of glucocorticolids on catecholamine synthesis in the heart and adrenals of rats in the presence of physical fatigue].

The influence of the adrenal cortex hormones on the catecholamine synthesis in the adrenal glands and the heart of rats following prolonged swimming (8 hours) was studied. Catecholamine synthesis after the incubation of the adrenal glands and heart in the presence of L-tyrosine was sharply inhibited after swimming. Addition of hydrocortisone or prednisolone in vitro (50 microgram per sample) and also administration of these hormones in vivo (50 mg/kg intramuscularly, 3 hours before decapitation) increased catecholamine synthesis in the adrenal glands of swimming, but not of intact rats. After the incubation of the adrenal glands of swimming rats in the presence of L-DOPA and L-noradrenaline, catecholamine synthesis was depressed in comparison with intact animals, and it failed to be restored on addition of glucocorticoids. No stimulating effect of aldosterone on catecholamine synthesis in the adrenal glands in the presence of L-tyrosine was revealed. Catecholamine synthesis was inhibited and not restored under the effect of glucocorticoids in vitro and in vivo after the incubation of the heart tissue of swimming rats in the presence of L-tyrosine and L-DOPA. A conclusion was drawn that glucocorticoid promoted restoration of catecholamine synthesis inhibiteds in case of strong physical fatique at the stage of tyrosin-hydroxylase.

Adrenal Glands↗
PubMed1989

[Essential hypertension caused by a virilizing adrenal tumor].

Authors report here an interesting case of a woman who has been treated for essential hypertension for 12 years. Beside the hypertension, an extreme virilization appeared. A large adenoma, originated from the left adrenal gland have been explored behind the clinical picture. After surgical removal of the adenoma, adrenocortical hormones decreased to the normal levels. Systemic blood pressure decreased considerably the virilisation showed gradual involution. The correct treatment of the patient was a decade late, resulting in the development of encephalopathic syndromes.

Adrenal Cortex↗
PubMed1995

Aldosterone: the minority hormone of the adrenal cortex.

In comparison with the glucocorticoids cortisol and corticosterone, the mineralocorticoid aldosterone is a minority hormone of the mammalian adrenal cortex, and its proper function is dependent upon protective physiological mechanisms. These include a particular site of aldosterone synthesis in zona glomerulosa cells as well as a complex multifactorial control system, which adapts aldosterone production to acute and chronic changes in body sodium and potassium contents, irrespective of pituitary ACTH secretion. In the course of the last few years, an important element of these mechanisms has been identified in the form of the enzyme involved in the final steps of aldosterone biosynthesis. In species such as the human, rat, and mouse, the conversion of deoxycorticosterone to aldosterone is catalyzed by an isozyme (CYP11B2) of cytochrome P450(11 beta) (CYB11B1). The gene encoding this enzyme is expressed only in the zona glomerulosa. Its transcription is enhanced by sodium deficiency and potassium intake, but is suppressed by long-term administration of high doses of ACTH. In contrast, the gene encoding CYP11B1, i.e., the major (non-aldosterone-producing) type of the enzyme, is expressed mainly in the zona fasciculata, and its expression depends on physiological concentrations of ACTH. In other animal species (cattle, pig), the major forms of cytochrome P450(11) beta have an inherent aldosterone-synthesizing activity, which is, however, selectively suppressed in mitochondria of zona fasciculata cells by yet unknown mechanisms.

Adrenal Cortex↗
PubMed1973

The role of protein kinase activation in the control of steroidogenesis by adrenocorticotrophic hormone in the adrenal cortex.

A method has been developed for investigation of the effect of adrenocorticotrophic hormone (ACTH) on the state of activation of a cyclic AMP-dependent protein kinase within cells of the adrenal cortex. Enzyme activity was measured in terms of the quantity of (32)P transferred from [gamma-(32)P]ATP to histone under conditions in which bound cyclic AMP did not dissociate from the regulatory subunit of the protein kinase ACTH (1x10(-2)i.u./ml) caused a rapid and complete activation of the cyclic AMP-dependent protein kinase activity within 2min of hormone addition to the isolated cells. In response to a range of ACTH concentrations a sigmoid log dose-response curve for protein kinase activation was obtained, with half-maximal stimulation attained at about 1x10(-3)i.u./ml. However, some low doses of ACTH that elicited a marked (but submaximal) steroidogenic response failed to cause a clear stimulation of protein kinase activity in isolated adrenal cells. Theophylline (2mm) potentiated the effect of ACTH on protein kinase activity. The results implicate an important role for protein kinase in ACTH action on the adrenocortical cell.

Adenosine Triphosphate↗
PubMed1995

Incidentally detected adrenal tumours (incidentalomas): histological heterogeneity and differentiated therapeutic approach.

OBJECTIVES: To find a differentiated therapeutical approach to incidentalomas. DESIGN: Prospective study of incidentalomas: their histology, hormonal activity, and growth if primarily non-operated. SETTING: Admissions to an academic tertiary care centre because of incidentaloma. PATIENTS: Thirty-eight female, 25 male, 27-85 years old. INTERVENTIONS: Ultrasound, computed tomography and adrenal scintigraphy when appropriate; investigations to exclude malignancy giving metastasis into the adrenal gland; ACTH, cortisol, aldosterone, renin activity, androgene, catecholamine measurements; surgery or follow-up. MAIN OUTCOME MEASURES: Rate of malignancy; linkage of tumour size to probability of malignancy; prevalence of tumours with subtle hormone excess. RESULTS: Cortical adenomas occurred in 13/31, metastases in 7/31 of the histologically confirmed cases. In 10/31 cases, the computed tomography indicated a size that was smaller than the pathological size (mean = 20 mm). 20.6% of all incidentalomas and 61.5% of the 13 operated corticol adenomas showed subtle hormonal activity. Twenty-seven incidentalomas < 30 mm were followed-up (3-41 months; mean 18 months) and showed growth in only one case. Sensitivity, specificity, and predictive value (PV) of a tumour > or = 30 mm to indicate malignancy were: 1.0, 0.56 and 0.27, respectively. The PV of a < 30 mm tumour to exclude malignancy was 1.0. CONCLUSIONS: Oncological screening tests are necessary in all incidentalomas. Tumours > or = 30 mm should be operated but smaller ones can be followed-up, because they are usually benign and rarely show progressive growth. Cortical adenomas with subtle hormonal overproduction and hypertension, diabetes or osteoporosis should be operated, irrespective of their size, but in the absence of relevant clinical symptoms they can be followed-up.

Adrenal Cortex Hormones↗
PubMed1996

Incidentally discovered adrenocortical adenomas are not fully nonfunctioning: immunohistochemical and dispersed adrenocortical cell study.

To clarify the precise function of incidentally discovered adrenocortical adenoma, immunohistochemical and dispersed adrenal cell studies were performed. We have recently seen five patients with so-called nonfunctioning adrenocortical adenoma. Diurnal variation in plasma cortisol and suppression of plasma cortisol and urine 17-hydroxycorticosteroids in response to dexamethasone administration revealed adrenocortical function within normal limits in all cases, and no signs or symptoms of adrenal steroid hormone excess were evident. Since a high uptake of iodomethylnorcholesterol was recognized in each adrenal mass, it was supposed that these adrenal tumors produced steroid hormone to a certain extent, and each patient received unilateral adrenalectomy. P450c17, a key enzyme involved in cortisol production, was expressed in the tumor region in all cases in an immunohistochemical study. Upon in vitro steroidogenesis with dispersed adrenal cells in two cases, all steroid hormones measured except for aldosterone (progesterone, 17 alpha-hydroxyprogesterone, pregnenolone, 17 alpha-hydroxypregnenolone, 11-deoxycortisol, cortisol, 11-deoxycorticosterone, corticosterone, 18-hydroxydeoxycorticosterone, dehydroepiandrosterone and androstenedione) were produced in a culture medium. The results indicated that these tumors possessed the capacity for cortisol production, which was in agreement with the results of an iodomethyl-norcholesterol scintigraphy. All patients with mild hypertension or diabetes mellitus had no signs or symptoms of steroid hormone excess, but they could potentially develop a steroid excess syndrome such as Cushing's syndrome in the future.

17-Hydroxycorticosteroids↗