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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extrarenal renin has been identified in a number of tissues, including the brain, the submaxillary gland, uterus, ovary, vascular endothelium, testes, pituitary gland, and the adrenal cortex. In some tissues, including the adrenal cortex, all of the components of the renin-angiotensin system have been identified; however, no specific physiologic role has been clearly demonstrated for these extrarenal renin-angiotensin systems. We have studied the role of the renin-angiotensin system in the adrenal cortex of the rat and have found that renin is localized and synthesized in the zona glomerulosa cells. Its production can be influenced by alterations in electrolyte balance, as well as the genetic background of the rat. In adrenal capsular explant cultures, a converting enzyme inhibitor can lower angiotensin II production and reduce the stimulation of aldosterone by potassium, suggesting that this system is involved in the aldosterone response to potassium. In addition to rat adrenals, renin has been identified in human adrenal tissue and human adrenal tumors, including aldosteronomas, and a patient with hypertension has been reported to have an adrenal tumor that appeared to be secreting renin into the circulation.
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PMID:Adrenal renin: a possible local regulator of aldosterone production. 269 84

A 37-year-old woman presented with hyperaldosteronism, suppressed renin levels, and a left adrenal mass on CT scanning. Selective adrenal venous sampling indicated a marked rise of the aldosterone level in the right adrenal vein, while the level in the left vein was low. On laparotomy, an aldosterone producing adenoma (APA) of 12x10x5 mm in size was found in the right adrenal gland and was resected, while the left mass was left in situ. The post-operative course showed normalization of both the clinical and biochemical features of primary aldosteronism, with no sign of recurrence or of enlargement of the remaining adrenal mass in 2.5 years of follow up, suggesting the possible coexistence of a "non-functioning" tumor. This case demonstrates the importance of adrenal venous sampling for the localization of APA particularly since the presence of the APA may be masked by a visualized but unrelated adrenal mass.
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PMID:Possible association of aldosterone producing adenoma and non-functioning adrenal tumor. 272 41

A 47-year-old female presented with hypertension, hypokalaemia, low plasma renin, high plasma aldosterone and was found to have a left adrenal tumour 4 cm in diameter by computerized tomography. Detailed biochemical studies showed high plasma levels of 11-deoxycorticosterone and corticosterone in addition to aldosterone and 18-hydroxycorticosterone. Basal 11-deoxycorticosterone levels were particularly high. Corticosterone, 18-hydroxycorticosterone and aldosterone concentrations were abnormally sensitive to infusions of ACTH and angiotensin II. Plasma cortisol and assays for sex hormones were normal although there was evidence that cortisol derived from the neoplasm. At operation a well-differentiated adrenocortical carcinoma weighing 50 g (56 X 30 X 36 mm) was removed. There was no evidence of metastases following surgery. Adrenal function returned to normal. Review of the literature suggests that adrenocortical carcinoma should be suspected in patients who otherwise have typical features of Conn's syndrome, but whose tumours are more than 3 cm in diameter. Measurement of steroids such as 11-deoxycorticosterone in addition to aldosterone is recommended since abnormally high values may also help to distinguish between hyperaldosteronism due to adenoma and carcinoma. Previously reported cases of isolated aldosterone production by a carcinoma cannot be substantiated.
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PMID:Hypermineralocorticoidism due to adrenal carcinoma: plasma corticosteroids and their response to ACTH and angiotensin II. 282 95

200 patients with mineralocorticoid hypertension were studied at the Clinical Study Center. The study of 150 patients with primary aldosteronism revealed five distinct subsets based on their responses to the upright posture, after administration of intravenous saline, deoxycorticosterone acetate, and spironolactone. Two new types were identified--aldosterone producing responsive adenoma (AP-RA) and primary adrenal hyperplasia (PAH). Patients with AP-RA maintained normal physiologic responses to the above maneuvers. Patients with PAH had responses similar to patients with an aldosterone producing adenoma (APA) but no tumor was identified. Both types were cured by unilateral adrenalectomy. There has been no change in subtype in up to 20 years of follow-up. The notion of a continuum from low renin hypertension to APA is not supported. Primary deoxycorticosteronism caused by a benign adrenal adenoma, malignancy and hyperplasia is described. Uniquely, overproduction of the 17-deoxysteroids of the zona fasciculata occurs with normal 17-hydroxy function. After the removal of a benign adenoma the contralateral adrenal gland revealed a delay in the 17-deoxysteroid responses to ACTH in the face of normal cortisol increases. This suggests that an independent pituitary regulator of the 17-deoxypathway may exist. Other hypertensive disorders with excessive deoxycorticosterone production are linked with increases of ACTH and cortisol levels. The hallmarks of primary deoxycorticosteronism are hypertension with hypokalemia, suppression of renin and aldosterone, and overproduction of the 17-deoxysteroids.
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PMID:Identification and implications of new types of mineralocorticoid hypertension. 291 10

A 26-year-old man with hypothalamic hypodipsia-hypernatremia syndrome is reported, who presented with adipsia, hypernatremia, and impaired osmolality-mediated arginine vassopressin (AVP) secretion. A chorionic gonadotropin-secreting tumor was detected in the anterior hypothalamus and treated with external irradiation. After the treatment, hypernatremia persisted and was not corrected by fluid loading, osmolality-mediated AVP secretion remained impaired. Despite the absence of signs of hydropenia, hypovolemia was suggested by low blood pressure and elevated plasma indices of the renin-angiotensin system, and supported by blood volume determination. The plasma aldosterone concentrations were inappropriately low for the renin-angiotensin status. The plasma atrial natriuretic polypeptide (ANP) level was normal in spite of hypovolemia and increased more than double after fluid loading. Hypernatremia, primarily caused by hypodipsia and impaired osmolality-mediated AVP secretion, secondarily sustained ANP secretion and suppressed aldosterone release, which conceivably contributed to the development and perpetuation of hypovolemia in this patient.
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PMID:Pathogenesis of extracellular fluid abnormalities of hypothalamic hypodipsia-hypernatremia syndrome. 297 77

Glucocorticoids have been postulated to directly inhibit adrenocortical steroid production in laboratory animals. To investigate this in the human, we measured specific [3H]dexamethasone-binding sites in cytosol samples from normal and neoplastic human adrenal tissues. All nine normal adrenocortical samples, six adenomas (four cortisol-producing and two aldosterone-producing), and two hyperplastic adrenocortical samples studied were devoid of measurable specific glucocorticoid-binding activity. In contrast, steroid binding with characteristics of the glucocorticoid receptor (concentration of binding sites, 32-146 fmol/mg cytosol protein; Kd, 1.7-3.1 X 10(-9) M) was readily detectable in cytosol of all three adrenocortical carcinomas and all three pheochromocytomas examined. To elucidate the in vivo role of glucocorticoids as direct regulators of adrenocortical function, five patients with hypopituitarism receiving varying oral maintenance doses of dexamethasone were given ACTH iv. Increasing the orally administered dexamethasone dose from 1 to 8 mg/day did not alter the plasma cortisol response to a 4-h infusion of 250 micrograms synthetic ACTH in these patients. Collectively, these data cast doubt on the proposal that synthetic glucocorticoids directly suppress adrenocortical function in the human. Whether glucocorticoid receptors in tumor tissue could mediate the dexamethasone-induced suppression of hypercortisolism occasionally reported in patients with adrenocortical neoplasia remains to be investigated.
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PMID:Glucocorticoid receptors and responsiveness of normal and neoplastic human adrenal cortex. 298 Dec 41

Adrenocortical carcinoma tissue removed from a mildly hirsute 16-year-old girl was cultured in order to assess steroidogenesis and responsiveness of the cells to adrenocorticotropic hormone (ACTH), human chorionic gonadotropin (HCG), and insulin. The cells in culture produced large amounts of androstenedione and testosterone; however, production of cortisol, which was initially high, decreased with time. No aldosterone, estrone, or estradiol was produced in vitro. Both monolayer cells maintained for 6 weeks and organ culture explants maintained for over 3 days responded to ACTH (10(-7) M) with increased production of androgens (testosterone, androstenedione, dehydroepiandrosterone) but decreased production of cortisol as measured by radioimmunoassay of steroids in the culture media. Concomitant with decreased cortisol production was the enhanced formation of 11-deoxycortisol in cells exposed to ACTH, suggesting impaired 11 beta-hydroxylation. Tissue exposed to HCG (10(-7) M) in organ culture showed an increase in androgen production over control levels, but no significant effect of HCG on glucocorticoid production was found. Tumor cells differed in their androgen response to ACTH and HCG, with enhanced adrenal androgens in the presence of ACTH and more gonadal-type androgens after exposure to HCG. Insulin exposure had no effect on production of either androgen or glucocorticoid by tumor tissue in organ culture. Thus, this adrenocortical carcinoma showed marked androgen production in culture which was enhanced in different ways by ACTH and HCG. 11 beta-Hydroxylation was impaired with time in culture. No specific effect of insulin on steroidogenesis was noted.
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PMID:Effects of adrenocorticotropic hormone, human chorionic gonadotropin, and insulin on steroid production by human adrenocortical carcinoma cells in culture. 299 Jun 78

The effect of synthetic alpha-human atrial natriuretic peptide (alpha hANP), a potent natriuretic and vasorelaxant polypeptide recently isolated from human atria, on aldosterone secretion was studied in vitro in collagenase-dispersed adrenal adenoma cells from a patient with primary aldosteronism. alpha hANP (3.2 X 10(-7) M) significantly inhibited both basal and potassium (16 mM)-stimulated aldosterone secretion, whereas it had little or no effect on aldosterone secretion submaximally or maximally stimulated by ACTH (3.4 X 10(-10)-3.4 X 10(-9) M) or angiotensin II (10(-8)-10(-9) M). The less potent effect of alpha hANP on aldosterone secretion by dispersed human adrenal tumor cells compared to that in in vitro animal studies may reflect decreased affinity and/or number of specific receptors for ANP on the tumor cells. Whether ANP plays a physiological role in regulation of aldosterone secretion in humans in vivo remains to be determined.
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PMID:Effect of synthetic human atrial natriuretic peptide on aldosterone secretion by dispersed aldosterone-producing adenoma cells in vitro. 299 43

A 56-year-old woman presented with intracranial hemorrhage. Laboratory examinations revealed severe hypertension, hypokalemia, elevated aldosterone excretion, and suppressed plasma renin activity. Left adrenocortical tumor was suspected and adrenalectomy was performed. The laboratory data after operation, however, showed no significant difference from the preoperative data. On the basis of further examinations, dexamethasone was administered and returned blood pressure to normal, and also normalized serum potassium, plasma aldosterone, and renin activity. The patient's illness was diagnosed as glucocorticoid-suppressible hyperaldosteronism. Light microscopically, the zona glomerulosa was hypertrophic and the outer zona fasciculata decreased in lipid droplets and was centrifugally arranged in small alveoli. Electronmicroscopically, the cells of the outer zona fasciculata had several lipid droplets and well-developed sER. Mitochondria were round to oval with lamellar or lamellovesicular cristae. These findings were evidence of hyperfunction. The cytoplasm of the cells also contained spironolactone bodies. Therefore, it is assumed that the aldosterone, which induced the disorder, was produced mainly in the outer zona fasciculata.
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PMID:Glucocorticoid-suppressible hyperaldosteronism. Ultrastructural observation of a case. 300 3

A 62-year-old man with small cell carcinoma (oat cell type) of the lung who had hyponatremia and renal sodium loss with inappropriate antidiuresis is reported. Plasma levels of arginine vasopressin (AVP) were not elevated inappropriately. Plasma levels of atrial natriuretic peptide (ANP), however, were high, and increased after water loading and hypertonic saline infusion. The renin-aldosterone axis was normal, as were adrenal, thyroid, and renal functions. Water restriction to 500 to 700 ml/d resulted in a rise in serum sodium. Analysis of the tumor tissue failed to demonstrate the presence of AVP or ANP. The findings (1) suggest that hyponatremia and renal sodium loss with inappropriate antidiuresis observed in the patient is due to an antidiuretic substance distinct from AVP, and (2) point to the possibility that hypersecretion of ANP may play a role in the pathophysiology.
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PMID:Hyponatremia in small cell lung cancer. Mechanisms not involving inappropriate ADH secretion. 303 97


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