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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The total non-conjugated plasma cortisol in 60 patients with hypertension disease (HD)is 17.5 mkg/ml. The free non-conjugated cortisol represents 8.45 per cent of the total - 1,5 mkg%, considerably (p less than 0.0001) higher than that in healthy subjects. Protein conjugated cortisol is 16.0 mkg%. The bounding capacity of transcortin the plasma of hypertonics is considerably decreased (p less than 0.0001) - 15.8 mkg (in healthy - 18.5 mkg) per 100 ml. ACTH level in the plasma of patients with HD is 32.0 pg/ml, considerably higher than that in healthy (25.8 pg/ml, p less than 0.0001). The elevation of the biologically active cortisol fraction in plasma of hypertonics is a function both of hypothalamo-hypopheseal stimulation and of transcortin level. That latent hypercortisolism is admitted to be manifestation of hypothalamo - hypopheseal superstimulation by increased ACTH secretion, in case of confirmed cerebro-hypothalamic disturbances in patients with hypertension disease.
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PMID:[Determination of free and protein bound cortisol, transcortin binding capacity and adrenocorticotropic hormone in the plasma of patients with hypertension]. 18 62

Locally recurrent, poorly differentiated carcinoma of the prostate was associated with hypokalemic alkalosis, marked hypernatremia, diabetes mellitus of recent onset, and hyperosmolar syndrome. These findings, with mild hypertension, in the absence of clinical features of Cushing's syndrome, suggested an ectopic ACTH syndrome. Plasma ACTH and cortisol levels were markedly elevated, and failed to suppress in response to either low or high-dose dexamethazone administration. The patient's condition deteriorated rapidly. Autopsy findings included carcinoma extensively infiltrating the prostate with extension to the urinary bladder, and metastases confined to the pelvic nodes and soft tissues. The adrenal glands weighed 23 g and showed diffuse hyperplasia. Extract of the prostatic tumor was analyzed for ACTH and showed approximately 40 times normal plasma levels (or about 4,010 pg/g of tissue); ultrastructural features showed secretory granules consistent with ACTH content of the tumor cells. Such cells were positive when stained for ACTH by peroxidase-tagged immunochemical methods. The case fulfills all established criteria for relating excess corticosteroid production and nonpituitary tumors.
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PMID:Ectopic ACTH, prostatic oat cell carcinoma, and marked hypernatremia. 19 43

A study was made of 77 patients with adiposity and a group of healthy persons with normal weight. Patients with adiposity had a significant increase of blood plasma aldosterone level; of decisive role in the formation of secondary hyperaldosteronism was played by the elevation of blood renin level. Apparently activation of the renin-angiotensin system and the associated intensification of mineralocorticoid function of the adrenal glands served as one of the causes of development of arterial hypertension in persons with excessive weight. In adiposity there proved to be an increased rate of cortizol secretion and of 17-OCS excretion with the urine; as to the blood plasma cortizol concentration, it failed to show any significant difference from the normal. Apparently stable blood cortizol level in the patients with adiposity was maintained as a result of intensified ACTH secretion; in these patients reserve possibilities of the adrenocorticosteroid function of the hypophysis were diminished.
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PMID:[Mineralocorticoid and glucocorticoid functions of the adrenal cortex and some mechanisms of their regulation in obesity]. 19 62

A 53-year-old male with Cushing's syndrome due to ectopic ACTH production from medullary carcinoma of the thyroid was reported. The clinical course and results of detailed endocrinological studies and immunohistochemical findings about the cancer tissue were described. An abnormally high concentration of calcitonin, ACTH and beta-MSH in both plasma and cancer tissue (thyroid, lymph nodes and liver) were documented by radioimmunoassay. Urinary 17-OHCS was as high as 38.4 mg/day and showed no supression following dexamethasone 8 mg/day administration. ORAL METYRAPONE (3 G/DAY) CAUSED NO RESPONSE IN URINARY 17-OHCS. Parallel increments in plasma calcitonin, ACTH and beta-MSH were observed following calcium and gastrin loading. Total thyroidectomy with modified radical neck dissection caused minimal changes of plasma levels of calcitonin, ACTH and beta-MSH and no improvement in the clinical manifestations of Cushing's syndrome. An aortogram revealed metastatic tumors in the liver. A second operation, total adrenalectomy, resulted in an improvement of the clinical and laboratory findings such as hypokalemia, high blood pressure, muscle atrophy and moon face. Immunofluorescent study showed different distribution patterns in calcitonin- and ACTH-positive cells in the primary focus but similar patterns in the liver metastasis.
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PMID:[A case of medullary thyroid carcinoma with ectopic ACTH syndrome (author's transl)]. 20 14

The renin-angiotensin-aldosterone system has been evaluated in 19 patients with Cushing's syndrome due to bilateral adrenal hyperplasia and in 2 patients with unilateral adenoma. In the first group urinary aldosterone was within the normal limits with a mean of 8.3 +/- 1.86 microgram/24 h. Aldosterone excretion did not change significantly after furosemide administration, ACTH infusion or dexamethasone. Upright PRA was suppressed in 9/16 patients with a mean of 4.9 +/- 1.85 ng/ml/3 h and showed only a slight response to furosemide. Dexamethasone alone did not produce any change. Both aldosterone and PRA were to some extent stimulated by an association of dexamethasone and furosemide. In the 2 patients with adenoma, aldosterone excretion was also normal, but PRA was very elevated. From our data it is concluded that in Cushing's syndrome due to bilateral hyperplasia, PRA and aldosterone excretion are partially suppressed. From our results on plasma deoxycorticosterone and corticosterone concentration it seems unlikely that these mineralocorticoids are the major cause of this phenomenon. However, it may not be excluded that other yet unidentified hormones could play some role in the pathogenesis of hypertension and renin suppression in Cushing's syndrome.
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PMID:Plasma renin activity and urinary aldosterone in Cushing's syndrome. 20 67

Starting from the interference between the renin-angiotensin-aldosterone (RAA) system and cardiovascular pathology in arterial hypertension (AH) we have made a correlative study of the cardiovascular system and plasmatic aldosterone in normal and hypertensive subjects under conditions of stimulation (ACTH) and inhibition (propranolol). After administration of ACTH (one of the physiologic mediators of stress) increased values for plasmatic aldosterone were found. Negative cardiovascular effect: arrhthmia, angor, AH, cardiac asthma, under the condition of preexisting cardiovascular pathology or altered steroidogensis, were also noticed. Inhibition with propranolol does not have conclusive effects in AH with normal aldosterone. The best effect were noticed in that hypertension which implies the RAA pressor system in its pathogeny, irrespective of etiology, the reduction AT occurring in parallel with decline in plasmatic aldosterone values and total peripheral resistance (RPT). Administration of propranolol in AH with activated RAA system irrespective of etiology represents a pathogenic treatment able to prevent efficiently the major complications of AH.
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PMID:Deviation of plasmatic aldosterone and significance of the stimulating (ACTH-cortrosyn) and inhibitory (propranolol) effects in hypertension and cardiovascular pathology. 20 29

Plasma renin activity (PRA) was measured in 14 control subjects and 27 patients with essential hypertension (EH) (low renin group: 9, normal renin group: 11, and high renin group: 7) before and after the following stimulation tests. Test procedures: 1) Circadian rhythm (0600, 1600 and 2400h). 2) Adrenal stimulation test (ACTH: 12.5 I.U.). 3) Adrenal suppression test (Dexamethasone: 1.0 mg). 4) Metopirone test (1.5 g). 5) Angiotensin II infusion test (8 ng/kg/min). 6) Saline infusion test (1000 ml/hr). Patients with low PRA showed significantly lower levels of PRA than those of other two groups in circadian rhythm, after 2 hours of ACTH infusion and after angiotensin II infusion. Furthermore, these patients showed significantly higher responses of PRA than other two groups after furosemide test under dexamethasone and after metopirone test. In case of saline infusion test, patients with low and normal PRA did not show significantly decreased levels of PRA after the infusion, though all patients with high PRA and all control subjects showed significantly decreased levels of PRA. From the present studies, it might be concluded that patients with low PRA has an unknown mineralocorticoid excess which is ACTH dependent and 11 hydroxylated and some of hypertensive patients have an abnormality in their renin-angiotensin-aldosterone volume feed back loop as a factor for hypertension.
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PMID:Pathogenesis of essential hypertension with low renin: responses of plasma renin activity to various stimulation tests in essential hypertension. 21 18

Hypertension in 17 alpha-hydroxylase deficiency was studied by comparing it with hypertension in Cushing syndrome or that in primary aldosteronism. Furthermore, the role of endogenous increases of ACTH, deoxycorticosterone, and 18 alpha-hydroxy-deoxycorticosterone upon blood pressure was studied in rats by administerating metopirone. Hypertension in 17 alpha-hydroxylase deficiency was considered to be more similar to that in primary aldosteronism from the studies on renin components, pressor responses to angiotensin II and norepinephrine, and renin responses to stimulations. Plasma catecholamines were slightly decreased in 17 alpha-hydroxylase deficiency. The hypertension was alleviated by the administeration of dexamethasone in 2 of 3 patients with 17 alpha-hydroxylase deficiency. However, in the remaining one who had an accelerated hypertension and normal renin, the hypertension was not alleviated by dexamethasone. In the animal studies, hypertension induced by metopirone was accelerated by salt loading of uni-lateral nephrectomy plus salt loading. In those rats, plasma ACTH, and deoxycorticosterone were markedly increased.
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PMID:Hypertension induced by adrenocortical dysfunction--hypertension in 17 alpha-hydroxylase deficiency and metopirone-induced hypertension. 21 19

As compared to fatty tissue cells of animals with normal pressure, those of SHR rats were found to be characterized by a higher lipolytic response and a larger increase in the cAMP content on exposure to the effect of ACTH. As compared to the controls, adrenalectomized SHR rats had an increased basal cAMP content and an increased lipolytic response of the adipocytes following adrenaline administration. In inhibition of phosphodiesterase in the fatty cells of adrenalectomized rats with normal pressure, the cAMP content grew by 20% as compared to that in SHR rats subjected to the operation. It is suggested that the changes in intracellular distribution of calcium, shown in this model of hypertension, may be the direct cause of the altered sensitivity of the "target" cells to the effect of hormones.
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PMID:[Mechanism of the change in adipocyte sensitivity to ACTH and adrenaline in spontaneous genetic hypertesion in rats]. 21 34

The effect of a 5 day ACTH test (40 U/24 h) on plasma aldosterone (aldo), deoxycorticosterone (DOC), plasma renin activity (PRA) and urinary excretion of aldosterone-pH1-conjugate (pH-1-aldo) and tetrahydro-DOC (TH-DOC) was investigated in 8 normotensive children (group I), 8 patients with hypertension of unknown origin (group II), and 4 hypertensive children with dexamethasone suppressible hyperaldosteronism (DSH) (group III). Changes in blood pressure and sodium balance were studied in all groups. Under baseline conditions there was no hormonal difference between group I and II. In contrast, the children in group III had a suppressed PRA and a 1.5--2 fold elevation of aldo and DOC. Plasma DOC and urinary THDOC increased continuously 10--50 fold in all groups during the ACTH test. Aldo rose transiently 2--4 fold on the first day of ACTH and fell subsequently below baseline levels in group I and II. The children with DSH (group III), however, showed an unusual, sustained aldo stimulation with ACTH. PRA decreased significantly after ACTH in group I and II. Sodium retention aTH administration. The highest blood pressure rise was observed in group III (from 124/72 to 139/90 mm Hg). The blood pressure response to ACTH was partly sodium dependent. Although aldo and DOC and sodium retention may contribute to the ACTH induced blood pressure elevation, other factors must play a role.
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PMID:Mineralocorticoids, salt balance and blood pressure after prolonged ACTH administration in juvenile hypertension. 21 19


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