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

The goal pursued has been to analyze clinical observations and hormonal studies of patients with empty sella turcica (EST), in order to review this disorder and determine if it can be considered a real syndrome. Fifteen patients with EST (3 men and 12 women) and mean age of 45.6 +/- 17.9 years have been prospectively studied. In the hypothalamus-hypophysis study, reserves of thyrotropin (TSH), prolactin (PRL), gonadotropins (FSH and LH), growth hormone (GH), adrenocorticotropin (ACTH) and cortisol were assessed. In addition, thyroid hormones and, for men, testosterone, were determined. The pathogenic mechanism was explained in two cases (13.3%). We registered headache in 10 patients, obesity in 8, arterial hypertension in 2 and diabetes mellitus in 2. Multiparity antecedent was found in 2 cases. The hormonal study was abnormal in two cases (40%). Most common abnormalities were hyperprolactinemia (3 cases), deficit of gonadotropins (3 cases), without coexisting both of them in any case, and deficit of GH (2 cases). EST is frequently associated with endocrine disfunction, although clinical implications are rare. The absence of common clinical manifestations in most cases questions the EST as a real syndrome.
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PMID:[Primary empty sella turcica: clinical aspects and hormonal study of 15 cases]. 179 Feb 77

An effect of the long-term prazosin therapy on sympathetic activity, renin plasma activity and beta-endorphin and lipid blood levels was investigated in 23 patients with the primary arterial blood hypertension. Group A included 18 patients treated with prazosin, and group B - 5 patients treated with prazosin combined with propranolol. Mean daily dose of prazosin in group A was 3.0-10.0 +/- 1.3 mg in different phases of therapy whereas in group B mean daily dose of prazosin was 3.0-6.5 +/- 1.8 mg and propranolol 50-80 mg. Significant decrease in diastolic and systolic blood pressure (p < 0.01) was achieved in both groups. Additionally significant decrease in pulse rate (p < 0.01) was seen in group B. It was found that prazosin produced significant increase in plasma noradrenaline in group A and decrease in 4-hydroxy-3-methoxyglycol excretion with the urine (p < 0.05) in both groups. Moreover, negative correlation between a decrease in blood pressure (diastolic) and noradrenaline excretion with the urine (p < 0.05) was noted in group A. No effect of prazosin therapy on plasma renin activity, beta-endorphin and lipids blood levels was observed in both groups. These results suggest that prazosin therapy in patients with the primary blood hypertension exerts an effect on sympathetic activity and does not change plasma renin activity or blood beta-endorphin and lipids levels.
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PMID:[Effect of long-term prazosin treatment on certain humoral and metabolic factors in patients with primary hypertension]. 184 64

The concentration of corticotropin-releasing hormone (CRH) in maternal plasma increases greatly during the last trimester of normal pregnancy. This CRH has been proposed to originate from the placenta. We studied plasma immunoreactive CRH in 46 uncomplicated pregnancies, in 10 pregnant women with chronic hypertension, in 17 women with pregnancy-induced hypertension (PIH) and in 24 women with pre-eclampsia, and correlated it to the levels of corticotropin (ACTH) and cortisol. CRH levels were greatly increased in women with pre-eclampsia, less significantly in women with PIH, while no change was found in pregnant women with chronic hypertension. ACTH levels also were increased in pregnancies with pre-eclampsia or PIH and there was a positive correlation between CRH and ACTH levels. CRH levels in cord venous plasma were significantly increased in pregnancies with pre-eclampsia but cortisol did not show any significant increase. These findings suggest that placental release of CRH into the maternal and fetal circulation is increased in pre-eclampsia.
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PMID:Corticotropin-releasing hormone in maternal and cord plasma in pre-eclampsia. 185 89

The paraventricular hypothalamus regulates autonomic nerve outflow and is innervated with beta-endorphin-immunoreactive nerve terminals. This study examined the effects of beta-endorphin microinjected into the paraventricular hypothalamus on blood pressure, heart rate, and plasma catecholamine and glucose concentrations in conscious, unrestrained spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats at the age of about 9 weeks. Thirty minutes after paraventricular hypothalamic injection of [125I] beta-endorphin (3.5 micrograms), most of the recovered radioactivity was detectable within +/- 0.5 mm from the injection site in the coronal, sagittal, and horizontal planes. Unilateral paraventricular hypothalamic injections of beta-endorphin (1 and 0.1 microgram/0.1 microliter) increased blood pressure and heart rate in both strains in a dose-independent manner with significantly greater increases in SHR. Plasma catecholamine and glucose concentrations were measured 15, 30, and 60 minutes after beta-endorphin injection. Norepinephrine concentrations were not significantly altered in WKY rats but increased in SHR. Epinephrine concentrations increased in both strains with significantly greater increases in SHR. Increases in catecholamine concentrations were not dose-related. Glucose concentrations also increased in both strains with significantly greater increases in SHR only at the lower dose. Ganglionic blockade with pentolinium significantly reduced beta-endorphin-induced pressor and tachycardiac responses in SHR. Pretreatment of the paraventricular hypothalamus with naltrexone (1.1 micrograms) in SHR blocked the initial pressor and tachycardiac responses to beta-endorphin (0.1 microgram) and blunted increases in epinephrine and glucose levels. When the animals were anesthetized with alpha-chloralose 2-5 days after the study in conscious animals, there were no differences in blood pressure or heart rate between strains after beta-endorphin (0.1 microgram) injection. The results indicate that conscious SHR show enhanced cardiovascular and sympathoadrenal responses to beta-endorphin injected into the paraventricular hypothalamus, suggesting that alterations in the activity of the paraventricular hypothalamic beta-endorphin system can modulate the development of hypertension in SHR.
Hypertension 1991 Oct
PMID:Sympathoadrenal control by paraventricular hypothalamic beta-endorphin in hypertension. 191 93

Among 436 patients with hypertension unrelated to any renal lesion, renovascular damage, pheochromocytoma, Cushing's syndrome or hyperthyroidism, 15 patients had low plasma renin activity (PRA) and elevated plasma aldosterone concentrations in the upright position and resultant high aldosterone/PRA ratios: 8 with aldosterone-producing adenoma (APA; group 1) and 7 with idiopathic hyperaldosteronism (IHA; group 2). Thirty-nine patients had suppressed PRA in the presence of normal plasma aldosterone levels and moderately elevated aldosterone/PRA ratios (group 3). Thirty of them had elevated plasma 11-deoxycorticosterone (DOC) and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) concentrations (group 3a) and 9 of them had normal levels of those mineralocorticoids (group 3b). The rest of them (382 patients) had low aldosterone/PRA ratios (group 4). Adrenal scintigraphy with dexamethasone pretreatment revealed [13I]-cholesterol accumulation not only in patients with APA (unilateral) or IHA (bilateral), but also in patients of group 3a (bilateral). In patients in groups 3a and 3b adrenal size (especially thickness), as measured by computed tomography (CT scan), was enlarged, as in patients with IHA (group 2), and was significantly greater than in patients of group 4 (p less than 0.001). Spironolactone reduced blood pressure in all tested patients of group 3a, and the removal of adrenal tumor or hyperplastic tissue normalized blood pressure in patients of groups 1, 2 and 3a. Excised adrenal glands exhibited cortical hyperplasia with or without nodular hyperplasia in patients of group 3a. Good agreement was found between the actual size of the excised tissue and the measurement obtained by CT scan. Since beta-endorphin and beta-lipotropin were depressed in patients of group 3a, it is suggested that an unknown pituitary substance stimulates the adrenal cortex to release too large amounts of DOC and 18-OH-DOC and inappropriate secretion of aldosterone.
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PMID:Inappropriate elevation of the aldosterone/plasma renin activity ratio in hypertensive patients with increases of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone: a subtype of essential hypertension? 207 Mar 75

The role of a high CRH level in normal pregnancy remains unknown. Therefore we evaluated the concentrations of CRH and the related hormones in patients with pregnancy-induced hypertension. Fourteen women with pregnancy-induced hypertension, aged 20-39, at 30-39 gestational week, were investigated. The control group consisted of 20 healthy pregnant women matched according to gestational age. Plasma CRH beta-endorphin-like immunoreactivity, cortisol, and human placental lactogen were measured by radioimmunoassay, ACTH by an immunoradiometric method. It was found that in hypertensive patients the mean CRH concentration was significantly higher (4257 +/- 840 (SEM) ng/l) than that in healthy pregnant women (1083 +/- 227 ng/l, p less than 0.001). The concentration of ACTH, however, was only slightly higher 65.0 +/- 6.0 vs 50.7 +/- 2.5 ng/l p less than 0.025, whereas the differences in beta-endorphin, cortisol and human placental lactogen were not significant. In both groups there was no correlation between the CRH level and those of the related hormones. In healthy pregnant women the CRH level closely correlated with gestational age (r = 0.76, p less than 0.001), whereas in patients with hypertension no such correlation was present (r = 0.29). We assume that the marked enhancement of plasma CRH in pregnancy-induced hypertension is probably caused by its decreased breakdown in ischemic placental tissue, but its increased synthesis in the placenta and its indirect counterregulatory hypotensive role must also be considered.
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PMID:Enhancement of plasma corticotropin-releasing hormone in pregnancy-induced hypertension. 214 45

Experiments characterized the dynamics of the pituitary and adrenocortical response to noise in awake dogs to determine if a dissociation exists between changes in plasma bioactive (bio) adrenocorticotropic hormone (ACTH) and immunoreactive (ir) ACTH. In addition, experiments determined the temporal relationship between cardiovascular, adrenomedullary, and adrenocortical responses induced by the acute presentation of noise. Trained dogs were prepared chronically with adrenal venous and femoral arterial cannulas. Experiments were done 48-96 h postsurgery and consisted of presentation of noise (75 dB; 0.25-8 kHz) for 3 min (n = 6) or of blood sampling alone (n = 5). In response to noise, mean arterial pressure and heart rate increased at 30 s and returned to base line at 4 min. Adrenal secretion of epinephrine and norepinephrine increased at 1 min and remained elevated until 4 min. Adrenal blood flow increased from 2 to 4 min as the result of a parallel increase in adrenal vascular conductance. Plasma bioACTH increased from 6 to 15 min in parallel with that of plasma irACTH. Before noise, the ratio of bioACTH to irACTH was 0.2-0.3, but the absolute change in bioACTH and irACTH after noise was not different. The increase in plasma ACTH occurred concomitant with or preceded an increase in cortisol secretion. Blood sampling alone caused no change in any variable. These data show that unexpected noise evokes a sequence of responses with rapid onset that includes tachycardia, hypertension, and increases in adrenomedullary secretion and adrenal vascular conductance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pituitary-adrenal and adrenomedullary responses to noise in awake dogs. 215 60

The response of plasma immunoreactive beta-endorphin (ir-beta E) and corticotropin to isometric exercise was studied in 10 women with pregnancy-induced hypertension (PIH) and in nine healthy women subjected to a handgrip test in the third trimester of gestation. The mean basal concentration of corticotropin was higher in the PIH than in the control group, 3.8 +/- 0.3 (SE) pmol/l and 2.2 +/- 0.2 pmol/l, respectively (p = 0.002). No significant difference was found in the basal ir-beta E level, 6.9 +/- 0.9 pmol/l and 6.1 +/- 1.0 pmol/l, respectively. In response to the handgrip test, the corticotropin and ir-beta E concentrations rose significantly in all subjects (p = 0.001 and p = 0.02, respectively) without any significant differences between the groups. These findings indicate that an isometric exercise is sufficient to increase the secretion of ir-beta E and corticotropin during pregnancy. Increased basal concentration of corticotropin in women with PIH may be explained by significantly increased circulating corticotropin-releasing hormone, 1451 +/- 323 pmol/l, as compared to 528 +/- 190 pmol/l in the control group.
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PMID:Response of plasma immunoreactive beta-endorphin and corticotropin to isometric exercise in uncomplicated pregnancy and in pregnancy-induced hypertension. 215 26

Beta-endorphin (B-Ep), ACTH plasma levels and cortisol serum levels have been evaluated by RIA, in 27 patients suffering from essential blood hypertension and in 20 healthy control subjects. The study was repeated in the hypertensive group after clonidine treatment for 15 days. B-Ep plasma levels were normal in the I stage of hypertension and did not show any significant difference in relation to the severity and duration of hypertension. ACTH and cortisol circulating levels in the hypertensive patients were in normal range. The increase of B-Ep plasma levels in the II and III stage of the hypertension is not modified by the reduction of blood pressure values; therefore it is unlikely linked to the elevated blood pressure, but probably to the vascular complications. Moreover, the results obtained after clonidine treatment seem to exclude that the hypotensive action of the drug is mediated by increment of B-Ep circulating levels.
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PMID:[Plasma levels of beta-endorphin and ACTH and serum levels of cortisol in different stages of arterial hypertension before and after clonidine therapy]. 216 79

To test whether angiotensinogen might be targeted to dense core secretory granules in cells containing a regulated secretory pathway, we expressed rat angiotensinogen in AtT-20 cells, a mouse pituitary cell line that has the demonstrated ability to correctly sort proteins to the constitutive or regulated pathway. We compared the pattern of secretion of angiotensinogen with that of endogenous adrenocorticotropin hormone, which is secreted by AtT-20 cells through the regulated pathway. When cells were incubated for 5 hours with dibutyryladenosine cyclic monophosphate or KCl, adrenocorticotropin hormone secretion was significantly higher than control, whereas monensin had no effect. In contrast, angiotensinogen secretion was markedly reduced by monensin, but no stimulation was observed with dibutyryladenosine cyclic monophosphate or KCl. These results make it unlikely that angiotensinogen could be cotargeted with active renin in the dense core granules of the regulated pathway. Alternative mechanisms must explain how angiotensin II is synthesized locally by tissue renin-angiotensin systems.
Hypertension 1990 Aug
PMID:Rat angiotensinogen is secreted only constitutively when transfected into AtT-20 cells. 216 1


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