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

In a genetically hypertension-prone (S) strain of rats it was observed previously that males generally developed hypertension more rapidly on a high salt diet than did females although final pressure ultimately were similar in both sexes. A genetic study had shown that there was no sex-linkage involved in setting blood pressure levels, so it was thought that the gonads might be involved. In the present work, castration of males had no effect on blood pressure but in the females it caused a rise in pressure that could not be distinguished from that in males, both on a high and low salt diet. Castration resulted in greater growth in females than in controls, whereas it had the opposite effect in males. It was speculated that these changes were due to influences on pituitary growth hormone with castration increasing the net output of growth hormone (or enhancing receptor sensitivity to it) in the female and the opposite in the male. From the work of others, there are some data compatible with such an interpretation. Experimentally, growth hormone will induce hypertension in rats. Therefore, it is conceivable that growth hormone is involved in the increment in hypertension observed in these castrate females. Because the effect on blood pressure was observed in castrate females on both high and low NaCl diets, it was considered unlikely that the blood pressure effect was simply due to increased NaCl intake in the food associated with greater growth. It was suggested that this rise in blood pressure with cessation of ovarian function might bear on the unsettled question of "menopausal" hypertension in women: in the genetically susceptible individual an increase in growth hormone associated with declining ovarian funtion in the menopause could provide the stimulus for the appearance of hypertension some years earlier than would otherwise have been the case.
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PMID:Role of the gonads in hypertension-prone rats. 116 74

Growth hormone (GH) hypersecretion is associated with an increased incidence of hypertension and cardiac hypertrophy, resulting in excess cardiovascular morbidity and mortality. Abnormalities in the renin-angiotensin-aldosterone (RAA) system have been reported in acromegaly and in normal adults treated with recombinant human GH. The RAA system was investigated in prepubertal children with idiopathic short stature during treatment with recombinant human GH in doses up to 40 IU/m2/week. In addition, left ventricular size and function were assessed by serial echocardiography over an initial 12-month period. Modest and transient increases in blood pressure and body weight were observed during the first 7 days of GH treatment, but this was not accompanied by activation of the RAA system. Echocardiographic parameters of left ventricular size and function remained within the normal range for age and body size. Short-term GH treatment of idiopathic short stature was thus not associated with an increase in risk factors known to be associated with later cardiovascular morbidity. Longer follow-up studies will be required to confirm the safety of high-dose GH in this respect.
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PMID:Growth hormone treatment in idiopathic short stature: a preliminary analysis of cardiovascular effects. 130 8

A 24 year old female with amenorrhea-galactorrhea due to a pituitary macroprolactinoma that eventually responded to bromocriptine with improvement of visual fields and intracranial hypertension syndrome is presented. After 2 years of treatment with bromocriptine her symptoms relapsed and she underwent transphenoidal hypophysectomy. The high serum prolactin levels detected initially decreased under bromocriptine to ward normal levels and was not modified after surgery, while gonadotropin production remain scarce. Growth hormone (GH) serum levels despite its normal concentration decreased significantly (p = less than 0.5) after pituitary ablation. We assume that the lack of response to bromocriptine in this case could have been due to a mixed hormonal nature of the tumor without overproduction or clinical expression of GH activity.
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PMID:[Macroprolactinoma resistant to bromocriptine]. 266 70

Cushing's syndrome in childhood is generally recognized by classical features such as truncal obesity, striae, easy bruising, moon facies, hypertension and growth retardation. Exceptionally, Cushing's syndrome has been reported to present as growth failure alone. We diagnosed transient hypercortisolism in 6 children who had poor growth as their only presenting abnormality. The 6 children all had integrated concentrations of cortisols (IC-F) (14.1 +/- 1.7 micrograms/dl; mean +/- 1 SD) which exceeded the IC-F in healthy children and adults (5.7 +/- 1.5 micrograms/dl; P less than 0.001). The IC-F of these 6 index cases overlapped the range of IC-F in patients with pathologically proven Cushing's syndrome (20.2 +/- 4.7 micrograms/dl). Four of the 6 patients were treated with human growth hormone for 8 months and showed a marked improvement in their growth rates. Four patients have entered puberty and are growing at normal rates. Three of the 6 children had normal repeat IC-Fs, subsequently, at a time they had normal growth rates. In 1-1/2 to 3 years of follow-up, none of the patients developed any other stigmata of Cushing's syndrome. We conclude that transient hypercortisolism, documented by the IC-F, may cause growth failure without other symptoms of Cushing's syndrome. Growth hormone therapy may improve the growth rate of these children at the time of their poor growth.
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PMID:Growth impairment due to transient hypercortisolism. 346 64

1. Growth hormone may influence cardiac growth during post-natal maturation or in response to hypertension, and the growth-hormone deficient dwarf rat model offers an opportunity to study this question. 2. We compared the blood pressure and heart weight of dwarf rats and Fischer (F344) control rats in early adulthood, after two hypertensive stimuli: unilateral renal ischaemia (two-kidney, one-clip) or the administration of deoxycorticosterone acetate and saline drinking fluid. 3. In untreated animals at 13 weeks of age the body weight of dwarf rats was significantly less than that of F344 rats, but the mean arterial pressure was similar. Although the hearts of dwarf rats were smaller than those of F344 rats, the heart weight/body weight ratio was significantly greater in dwarf rats. 4. Both dwarf and F344 rats developed similar hypertensive mean arterial pressures 5 weeks after left renal artery clipping or treatment with deoxycorticosterone acetate salt. The heart weights of hypertensive dwarf and F344 rats were equivalent, indicating a proportionally greater increase in cardiac size in dwarf rats for the same rise in blood pressure. 5. The plasma insulin-like growth factor-I level was markedly lower in dwarf than in F344 rats, and hypertension did not have any significant effects on these levels. 6. These findings indicate that the developmental increase in blood pressure and heart size in growing animals and the adaptive cardiac hypertrophy accompanying hypertension are not affected by growth hormone deficiency.
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PMID:Hypertension and cardiac hypertrophy in growth hormone-deficient rats. 792 70

In order to determine whether acromegaly is still associated with increased mortality, a hospital case note review of all patients with acromegaly followed up in Stoke-on-Trent since 1967 was carried out. Of 79 subjects identified, 51 are alive and being monitored and 28 have died. Mortality was compared to the general population by life table analysis. Secretion of growth hormone was assessed and compared in dead and alive patients. The effect of diabetes, hypertension, and growth hormone secretion on long-term outcome was assessed. Acromegaly is still associated with increased mortality, with an overall ratio of observed to expected deaths equal to 2.68 (95% C.I. 1.8-3.9; p < 0.001), but the survival of 31 (39%) patients whose growth hormone level had been reduced to below 5 mU/l was equal to that of the general population (O/E = 1.42; 95% C.I. 0.46-3.31: p > 0.05). The dead patients had had significantly higher growth hormone levels than those still alive, but mortality did not appear to be influenced by diabetes or hypertension. The cause of death was vascular in 57% of cases. Growth hormone hypersecretion is still associated with excess mortality in acromegaly. The present study suggests that the therapeutic objective should be to lower average daytime growth hormone levels to less than 5 mU/l. There is need for a large study to compare different modes of treatment in terms of their effect on growth hormone secretion and on long-term outcome.
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PMID:An audit of outcome of treatment in acromegaly. 832 47

Growth hormone (GH) insensitivity is a pathological state characterized by a disturbance of the physiological relationship between GH secretion, synthesis of insulin-like growth-factor I (IGF-1) and the biological actions of GH. Laron syndrome, the prototype for GH insensitivity, is most often due to GH receptor deficiency. However, this syndrome is heterogeneous in terms of growth characteristics, bio-chemical features and, most importantly, genetic defects. Recent data have indicated that partial GH receptor deficiency could be involved in children with apparently idiopathic short stature. Laron syndrome, because of extreme growth deficiency and a lack of alternative treatment, was the first clinical situation in which recombinant human IGF-1 was used. IGF-1 accelerates growth rate in most patients, induces subtle modifications of the craniofacies and decreases fat mass. However, it is still too early to evaluate the long-term effects of IGF-1 on final height. Tolerance to the drug has been excellent in all reported trials. The major (but rare) side effects are transient intracranial hypertension and hypokalemia. Generalization of data obtained in Laron syndrome to other clinical situations should take account of the profound alterations in IGF-1 pharmacokinetics resulting from a deficiency in IGF-binding proteins.
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PMID:Growth hormone insensitivity syndrome (Laron syndrome): main characteristics and effects of IGF1 treatment. 876 71

The purpose of this study was to evaluate the mortality experience of persons with longstanding diabetes who had received pituitary irradiation for diabetic retinopathy compared to a matched group of persons with diabetes who had not had pituitary ablation. The irradiated cohort consisted of 167 patients treated at the Donner Pavilion (Lawrence Berkeley Laboratory, University of California, Berkeley), and the comparison cohort was the population evaluated in the Wisconsin Epidemiologic Study of Diabetic Retinopathy (WESDR). Survival analyses were performed comparing the two cohorts using three different sets of matching criteria, each more restrictive than the previous analyses. The three different strategies were (1) matched only on severity of diabetic retinopathy; (2) matched on severity of retinopathy and age; and (3) matched on severity of retinopathy, age, gender, and hypertension status. Tests of comparison were the log-rank test, the Wilcoxon test, and the likelihood ratio test. For the model matching only on severity of retinopathy, mean survival was 8.3 years for the WESDR group and 9.4 years for the ablated group (p > 0.05 for all three statistical tests). For the model matched on retinopathy and age, mean survival was 8.9 years for the WESDR group and 9.2 years for the ablated group (p=0.05 log-rank test, 0.32 Wilcoxon test, and 0.06 likelihood ratio test). For the model matching on retinopathy, age, gender, and hypertension status, mean survival was 8.9 years for the WESDR group and 11.6 years for the ablated group (p=0.72 log-rank test, 0.08 Wilcoxon test, and 0.82 likelihood ratio test). These data are compatible with the notion that pituitary ablation, and therefore induced pituitary growth hormone deficiency, may not decrease survival in those with severe diabetic retinopathy.
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PMID:Survival following alpha particle pituitary irradiation for diabetic retinopathy. 974 40

Many factors contribute to the growth failure of chronic renal failure: water and electrolytes disturbances, hypertonicity, phosphate or calcium wasting, secondary hyperparathyroidism, anemia, hypertension, metabolic acidosis, and malnutrition. In addition, the pubertal growth spurt is usually stunted. Growth hormone (GH) resistance is observed with low GH binding protein (GHBP) level, and normal or low IGF I levels despite elevated GH level. Elevated IGFBP levels may contribute to a reduced IGF activity, especially in dialysed patients. Glucocorticoid therapy in transplanted patients further contribute to poor growth and inhibited IGF I activity. As conventional treatments have a limited effect to improve growth, adult height is often far below -2 SD. GH therapy has proved to be successful, especially in young children, overpassing the hormonal resistance so that an adult height within the normal range may be reached.
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PMID:[Physiopathology of the somatotropin axis in chronic renal insufficiency]. 985 82

The spontaneously hypertensive rat (SHR) is a widely used animal model for the study of hypertension. It also exhibits an osteonecrosis of the femoral epiphysis that resembles the clinical features of Perthes' disease in humans. In this rat model, occlusion of the epiphyseal vessels occurs as a result of a breakdown of the mechanically vulnerable epiphysis. The postnatal development of the epiphysis recapitulates the serial events of the endochondral ossification (i.e., cartilage formation), chondrocyte hypertrophy, cartilage mineralization, vascularization, and introduction of osteoblasts that form the secondary ossification center within the epiphysis. In the present study, a detailed radiographic and histological analysis demonstrates that the osteonecrosis is preceded by a disturbance of the cartilage mineralization and a disturbance of the ossification, despite a normal hypertrophy of the epiphyseal cartilage. These observations suggest that abnormal development of the femoral epiphysis occurs much earlier than manifestation of the osteonecrosis. They lead us to a hypothesis that yet-unclarified transitional events between the cartilage hypertrophy and the cartilage mineralization may be affected in SHRs. Type X collagen is a developmentally regulated matrix molecule that is implicated in the mineralization of the hypertrophied chondrocytes. We show that the expression of type X collagen during epiphyseal ossification is delayed in SHRs (vs. normal controls), suggesting disturbed growth and/or differentiation of the epiphyseal chondrocytes. Postnatal growth and differentiation of the chondrocytes at least partly depend on insulin-like growth factor-I (IGF-I), which is produced by the chondrocytes in response to the pituitary growth hormone and stimulates cartilage growth in situ. The present study demonstrates an altered IGF-I expression during early postnatal life in SHRs and suggests that the altered IGF-I expression as well as the following delay in upregulation of type X collagen may cause the mechanical vulnerability of the femoral epiphysis in SHRs.
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PMID:Altered postnatal expression of insulin-like growth factor-I (IGF-I) and type X collagen preceding the Perthes' disease-like lesion of a rat model. 1064 20


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