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

Of 103 borderline essential hypertensives below the age of 36 years, 11 (10.7%) showed low renin, 57 (55.4%) showed normal renin, and 35 (33.9%) showed high renin. Various hormones such as plasma catecholamines, PA, DOC, B, cortisol 18-OH-DOC, 18-OH-B, ACTH, AVP and PRL tended to be high in the high renin group and tended to be low in the low renin group. Furthermore, urinary excretion of kallikrein was also increased in the high renin group and reduced in the low renin group. There was no hormone which was increased in the low renin group. Regardless of renin levels, pressor responses to exogenous angiotensin II were increased in these juvenile essential hypertensives. From these studies on endocrine factors it is concluded that essential hypertensives are largely divided into 3 groups; the high hormone group, the normal hormone group and the low hormone group, and increased hormones may play an important role in the development of hypertension in the high hormone group. However, in the low hormone group and a part of the normal hormone group the mechanism of hypertension cannot be revealed by the study on endocrine factors.
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PMID:Endocrine factors in juvenile essential hypertension. 675 Jan 91

Hypertension-prone, male, spontaneously hypertensive rats (SHR; n = 60) and normotensive, male, Sprague-Dawley rats (S-D; n = 60) were exposed to the relatively innocuous stimulus of heat and ether when they were 40 days of age, just before the usual onset of high blood pressure in SHR. The animals were decapitated 0, 2, 5, 15, and 60 min postexposure to heat and ether. Blood levels of corticosterone, aldosterone, PRL, GH were measured concomitant with pituitary content of GH and PRL and adrenal content of ascorbic acid and cholesterol. The foregoing constituents were used as an index of pituitary-adrenal responsiveness. Changes in circulating corticosterone, PRL, GH, and especially aldosterone indicated that before the onset of their high blood pressure, SHR are much more responsive to noxious stimuli than normotensive S-D. The pattern of change in the pituitary content of GH and PRL, adrenal ascorbate, and cholesterol were also indicative of SHR hypersensitivity. These findings suggest that adrenal steroidogenesis and the stress response pattern in SHR vs. normotensive rats may be unique.
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PMID:Hypersensitivity of spontaneously hypertensive rats to heat and ether before the onset of high blood pressure. 684 14

The responses to immobilization, ether, and heat of spontaneously hypertensive rats (SHR) and normotensive Sprague-Dawley rats (S-D) were compared. Hyperglycemia reached a maximum within 5 min of exposure and was most intense in SHR. There were no differences in the pituitary content of GH or PRL between the SHR and S-D. Circulating GH levels were especially depleted in SHR 15 min post exposure, with rebound to high blood levels at 1 h. Circulating PRL levels were slightly higher in quiescent SHR vs. S-D but surged to much higher levels post exposure in SHR vs. S-D. Postexposure blood corticosterone and aldosterone levels rose to much higher levels in SHR vs. S-D. Although the blood glucose, GH, PRL, corticosterone, and aldosterone levels are similar in hypertensive SHR and normotensive S-D under quiescent conditions, SHR appear to be much more sensitive and respond more vigorously to heat, ether, and immobilization. It is suggested that abnormal activity of the hypothalamic-pituitary system may play a role in the pathogenesis of the genetically programmed hypertension of SHR.
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PMID:Hypersensitivity of spontaneously hypertensive rats (SHR) to heat, ether, and immobilization. 721 95

The effects of d-Sulpiride (25 mg i.v.) and 1-Sulpiride (25 mg i.v.) administration in the control of arterial blood pressure (ABP) and PRL-GH secretion have been analyzed in five normal male volunteers. It was observed a quite different action on ABP, 1-Sulpiride causing a long lasting hypotension and d-Sulpiride a short-lived hypertension. The correlation between ABP, heart rate and PRL-GH levels suggests a probable central cation for 1-Sulpiride and a possible peripheral action for d-Sulpiride effects on ABP.
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PMID:[Effects of sulpiride isomers in the control of blood pressure in man]. 745 1

Primary empty sella syndrome (ESS) is an anatomo-radiological picture characterized by the presence of an arachnoid herniation filled with liquor that compresses the pituitary against the sellar wall. ESS occurs particularly in obese, hypertensive, cephalalgic women. It is often asymptomatic but may be associated with ophthalmologic, neurologic and non-characterizing endocrine disorders. We report here 43 cases of primary ESS observed and assessed in our Departments of Internal Medicine from June 1983 to May 1993. The following endocrinological diagnostic procedures were carried out: hormonal (RIA) basal profile: FT3, FT4, TSH, PRL, ACTH, FSH, LH, 8.00 a.m. and p.m., blood cortisol, aldo, PRA, DHEA-S, FTe, E2, P, PTH, CT, and calcemia and phosphoremia; provocative tests: TRH, GnRH, etc.; inhibition tests: high dose dexamethasone. Clinical, neurologic (skull radiographs, sellar stratigraphy, computed tomography scan and magnetic resonance), and ophthalmologic (fundus, visual fields) assessments were also made. Our findings fit with the data in the literature concerning common symptoms of ESS, associated endocrinopathies and other illness. We found obesity (62.7%), oligo-amenorrhea (16.6%), galactorrhea (14.6%), hyperPRL (11.6%), hypopituitarism (9.3%), hypogonadism (4.6%), diabetes insipidus (2.3%), (micro-)polycystic ovary syndrome (19%), hyperACTH (2.3%). In 9.3% of the cases, endocrinopathy referred to pituitary adenomas. Moreover, we noted a high frequency of psychological disorders, to our knowledge not previously reported in the literature, including anxiety or dysthymic disorders with altered behavior (chiefly oral compulsion). We also make the hypothesis that obesity (occurring in 62.7% of our patients) and hypertension (62.7%) may be related to hypothalamic alterations.
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PMID:[43 cases of primary empty sella syndrome: a case series]. 761 55

Primary empty sella syndrome (ESS) is an anatomo-radiological picture characterized by the presence of an arachnoid herniation filled with liquor that compresses the pituitary against the sellar wall. ESS occurs particularly in obese, hypertensive, cephalgic women, it is often asymptomatic but it may be associated with ophthalmologic, neurologic and sometime non-characterizing endocrine disorders. We report here 71 cases of primary ESS observed and assessed during the last fourteen years. The following endocrinological diagnostic procedures were carried out: hormonal (RIA) basal profile: FT3, FT4, TSH, PRL, ACTH, FSH, LH, 8.00 a.m. and p.m. cortisolemia, Aldo, PRA, DHEA-S, FTe, E2, P, PTH, CT, and calcemia and phosphoremia; provocative tests: TRH, GnRH, insulin hypoglycemia, etc.; inhibition tests: "overnight" and high dose dexamethasone. Clinical, radiological (skull radiographs, CT and/or MRI) and ophthalmologic (fundus, visual fields) assessment were made. We found principally cephalgia (52/71: 73.2%), hypertension (42/71: 59.1%), obesity (47/71: 66.1%). But we found especially mental disorders (57/71: 80.2%), in our knowledge not previously reported in the literature, as anxiety or dysthymic disorders with behavioural disturbances (chiefly oral compulsion). We found endocrinopathies in 36/71 (50.7%), isolated or coexisting in some patients: hyperPRL (14%), hypopituitarism (10.4%), hypogonadism (7%), diabetes insipidus (2.8%), hyperACTH (1.4%), hypoGH (15.4%), pituitary adenomas (8.4%). Several hypothalamic illness show a clinical picture including mental disorders and obesity. The Authors hypothesize that the ESS may be a "new" hypothalamic syndrome (compression/stretching on hypophysis and/or hypophyseal stalk by arachnoidocele; disorder of some hormones and neurotransmitters as leptin, neuropeptide Y, orexins, POMC-derived peptides, etc).
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PMID:[Primary empty sella syndrome. Observations on 71 cases]. 1020 96

Hypertrichosis, characterized by increased hair growth located in non-androgen-dependent areas, does not justify the monitoring of hormone levels, conversely to hirsutism, with increased hair growth in androgen-dependent areas of the female genitals. Adult hypertrichosis is iatrogenic (minoxidil, ciclosporine, diazoxide or glucocorticosteroids), of metabolic origin (porphyria), nutritional (anorexia) or paraneoplastic (hypertrichosis lanuoginosa). Metabolic or general assessment can help clinical diagnosis. In non-iatrogenic hirsutism the following must be eliminated: 1) a virilizing tumor (ovarian, adrenal) when confronted with rapid progression or recent hirsutism, plasma testosterone (T)>1.5ng/ml and/or (adrenal tumor) DHEA-sulfate (DHEAS)>700 microgram/dl and associated with hypertension; 2) when confronted with characteristic signs of hirsutism, Cushing's syndrome (post-dexamethasone cortisol), hyperprolactinemia (pooled PRL), or acromegalia (IGF1). Measurement of 17-OH-progesterone at 8 am on the 4th day of the cycle detects the late manifestation homozygous forms of a 21-hydroxylase (21OHD) block. The more frequent forms are: 1) ovarian polymicrocystic or hirsutism-anovulation syndromes without other causes (LH/FSH, T, hyperinsulinemia, sonography); 2) functional adrenal hyperandrogenia (increased DHEAS without organic cause); 3) idiopathic hirsutism. Treatment can be local (discoloration, depilation, diathermo-coagulation, laser). Treatment of hirsutism of organic origin is etiologic. The inhibitory effects of glucocorticosteroids are mediated by 21OHD. The most effective treatments are anti-androgenic: cyproterone acetate, progesterone-like and anti-gonadotropic (contraceptive) agents; and the only product in France officially indicated in hirsutism , spironolactone (anti-mineralocorticosteroid); and flutamide, pure anti-androgen (probably hepatoxic). Finasteride (type II 5 alpha-reductase inhibitor) appears less effective. Estrogen-progestagen-like agents can be associated with anti-androgens. We should also mention the GnRH-agonists, and finally, dietetics and metformine (in cases of insulin-resistance).
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PMID:[Hirsutism and hypertrichosis in adults: investigations and treatment]. 1222 63

We report a 45-year-old woman with Cushing's syndrome showing reversible pituitary dysfunction. Left adrenal tumor was incidentally discovered by a screening examination of abdominal computed tomography. Although this patient lacked typical Cushingoid features except hypertension and leg edema, endocrine examinations revealed moderate suppression of plasma ACTH (~6.3 pg/ml) with relatively high levels of serum cortisol (~22.9 microg/dl) without normal circadian rhythm. Plasma ACTH failed to respond to either CRH or metyrapone, and dexamethasone failed to suppress her daily steroid production. Surgical removal of left adrenocortical adenoma and 6-month replacement of hydrocortisone have ameliorated both ACTH and cortisol responses to CRH loading test. Postoperative responses of TSH and GH to TRH and GRH, respectively, were two fold higher than the preoperative levels. In contrast, basal and TRH-induced levels of serum PRL were decreased after surgery although both the basal and stimulated PRL levels were markedly high before surgery. In addition, gonadotropin response to GnRH examined in the same ovarian cycle was decreased in accordance with an increase in serum estradiol and progesterone levels after surgery. Improvement of hypercortisolemia even in a moderate case of Cushing's syndrome not only ameliorates hypertension, obesity and glucose intolerance, but also restores the accompanying dysfunctions of anterior pituitary, suggesting the clinical importance of early discovery and treatment of functioning adrenocortical incidentalomas.
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PMID:Reversible pituitary dysfunction in a patient with Cushing's syndrome discovered as adrenal incidentaloma. 1511 71

Fetal growth retardation is a result of a complex pathology caused by multiple factors of fetal, placental, and maternal origin. Hormones and growth factors released as a result of maternal-fetal physiological interactions play an importance role in fetal well being and fetal outcome. Intrauterine Growth Retardation (IUGR) is associated with significant perinatal and childhood morbidity. It is estimated that 13.7 million infants are born annually with IUGR, comprising 11% of all births in developing countries. Both maternal malnutrition and anemia are associated with various degrees of fetal growth retardation. The relationship between decreasing birth weight percentiles and increasing fetal morbidity and mortality has been demonstrated by several investigators and epidemiological studies suggest that IUGR is a significant risk factor for the subsequent development of chronic hypertension, ischemic heart disease, diabetes, and obstructive lung disease in adult life (Barker's Hypothesis). Maternal anemia and/or malnutrition are recognized to be the most frequent cause of IUGR and SGA birth in developing countries like India. In order to investigate adaptive mechanisms by the fetus to overcome the growth disadvantage caused due to maternal nutritional limitations, we examined the quantitative variations in hormonal and growth factor profiles in paired cord blood and maternal samples obtained from neonates born to malnourished and/or anemic mothers. The results of our study show that: 1) The percentage of small for gestational age (SGA) neonates born to malnourished and anemic mothers was significantly higher than those born to mothers who were either malnourished or anemic; 2) Significantly higher levels of GH, PRL, HPL and IGF-1 were observed in the cord blood of neonates born to malnourished and anemic mothers indicative of an adaptive response on part of the fetus to over come an in-utero growth disadvantage; 3) The anoxemia-related fetal perturbations may have unique features that make them distinct from nutrient deficiency-related IUGR. Thus, these novel observations are relevant to the context of the ongoing scientific debate on Barker's hypothesis.
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PMID:Effect of maternal malnutrition and anemia on the endocrine regulation of fetal growth. 1547 29

Multiple endocrine neoplasm type 1 (MEN1) syndrome predisposes to the development of endocrine and non-endocrine tumors with an autosomal dominant pattern of inheritance. Different mutations have been found throughout the gene with a variable phenotype expression. The proband, a Caucasian man, was admitted to our department in 2001, at the age of 51 because of a 1-yr history of diarrhoea and hypertension. He reported a previous intestinal resection for bowel occlusion with a histological diagnosis of unspecified mesenchymal neoplasia. He had also undergone a left adrenalectomy for a large nonfunctioning adrenal adenoma. Subsequently, he had suffered from gastralgia and melena; a gastroduodenoscopy showed an erosive gastritis. His family history was negative for endocrine disorders. On physical examination, multiple abdominal cutaneous lipomas and facial angiofibromas were observed. Biochemical screening revealed a primary hyperparathyroidism and an increase in circulating levels of PRL, chromogranin-A, gastrin and glucagon. The whole body computed tomography (CT) scan, the 111In-octreotide scan and the pituitary magnetic resonance imaging (MRI) did not reveal any abnormality. The presence of small neuroendocrine tumors was suspected by a positron emission tomography uptake in the epigastric region. The endoscopic ultrasound revealed a pancreatic lesion sized 1.1 cm that is under evaluation. Direct DNA sequencing analysis of the proband MEN1 gene revealed the 579delG frameshift mutation in the exon 3. The genetic screening of the family revealed the same mutation in 3 out of 5 offspring. The biochemical screening revealed some features of the MEN1 syndrome in all three of them. In conclusion, a novel frameshift MEN1 mutation was found in kindred with an apparently negative family history. Our experience confirms that MEN1 syndrome is a complex and underestimated condition, unless specifically investigated by trained specialists.
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PMID:MEN1 family with a novel frameshift mutation. 1679 69


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