Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogenic compounds are the most important group of drugs that can induce hypertension. Studies have shown an incidence of significant hypertension amounting to less than 1% after 1 year of taking oral contraceptives and about 2% after 5 years. The ratio of the incidence of hypertension among ''takers'' to that of ''nontakers'' has been assessed at 1.8 by 1 study and 2.6 by another. Small but significant increments in systolic and diastolic pressures can be discerned during the first 2 years of treatment. Cessation of treatment has resulted in pressures returing to pretreatment levels within 3 months. In those previously normal the highest readings during oral contraceptive use were only 155/90 mm of Hg. Severe hypertension is more likely to occur in the predisposed, and malignant hypertension has been reported. Previous hypertension, toxemia of pregnancy, obesity, and nephropathy are predisposing conditions. Although progestagens, used alone, do not cause clinical hypertension the incidence of hypertension associated with an estrogen-progestogen combination was directly related to the dose of progestagen used. Weight gain is often observed in oral contraceptive users and is occasionally accompanied by edema and hypertension. There is a marked increase in the circulating level of renin substrate (angiotensinogen) which is caused by the estrogen component of the pill. The increase in renin substrate is associated with increase in plasma levels of renin activity, angiotensin 2, and aldosterone, together with a fall in plasma renin concentration. The suppression of plasma renin concentration can persist for weeks after stopping the pill. The factors responsible for hypertension are probably intrinsic and may be either neural, vascular, or renal. Patients taking oral contraceptives should have blood pressure checks at 6-month intervals, and more frequently in high risk cases. In the management of those with only mild blood pressure elevation, such patients should change to a preparation with the lowest available estrogen dosage, 30 mcg of ethinyl estradiol, or reserve the method for use during crucial periods of family planning. With moderate hypertension the oral contraceptive should be suspended for 3-6 months. If the blood pressure falls, oral contraceptives should not be resumed but another method recommended. Continuing hypertension requires further study and possibly elective sterilization. Severe hypertension requires withdrawal of the pill, urgent investigation, and treatment. Other drugs may cause hypertension. Management of these patients is outlined. Structural formulae of progesterone, norethisterone acetate, medroxyprogesterone acetate, and norgestrel are shown.
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PMID:Drug-induced hypertension: pathogenesis and management. 18 40

The 24-hour variations in the corticotropine, cortizol, thyrotropin, thyroxin, renin, aldosterone, and somatotropin secretion were studied in patients with obesity with the excess of body weight of 51--133% (84.7 + 7.8%) and in healthy persons of normal weight. Obesity proved to be accompanied by marked disturbances of the 24-hour variations of corticotropine, cortizol, thyrotropin, thyroxin, renin, and aldosterone. Unequally marked shifts in 24-hour variations in the secretion of various hormones indicated different changes in the corresponding structures of the hypothalamus during the obesity development. Changes in 24-hour variations in corticotropine and cortizol secretion were in the same direction in alimentary-constitutional and hypothalamic obesity.
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PMID:[Daily variations in the secretion of several hormones in obesity]. 21 84

1. Variables involved in the genesis of hypertension in male broad-breasted white turkeys include social environment, obesity and high salt intake. 2. The hypertension is characterized by low plasma renin activity and, with increasing age, normal to high plasma aldosterone. 3. Medionecrosis of the abdominal aorta is a common pathological finding. 4. The absence of atherosclerotic plaques is probably related to the high concentrations of alpha-lipoproteins.
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PMID:The natural history of hypertension in turkeys. 28 53

The separate steps in the formation of aldosterone from cholesterol were studied in a strain of spontaneously hypertensive rats in which phenotypic obesity is inherited as a recessive trait (Koletsky rats). The obese and hypertensive state had little or no effect on side-chain cleavage of cholesterol, formation of progesterone from pregnenolone or 21-hydroxylation. Mitochondrial 18-hydroxylation of endogenous and exogenous corticosterone, however, as well as 18- and 11 beta-hydroxylation of deoxycorticosterone, were increased in obese hypertensive rats, both when compared with non-obese hypertensive siblings and when compared with healthy Sprague-Dawley rats. 18-Hydroxylation of corticosterone was increased more than 18-hydroxylation of deoxycorticosterone. In non-obese hypertensive rats, the adrenal content of mitochondrial cytochrome P-450 was lower than that in obese hypertensive rats but higher than that in rats of the conventional Sprague-Dawley strain. The results are discussed with respect to possible heterogeneity of adrenal cytochrome P-450 and to possible explanations for the changes observed.
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PMID:Adrenal hydroxylations in genetically obese and hypertensive rats. 48 14

A method is presented for radioimmunological determination of 3alpha, 5beta-tetrahydroaldosterone. It is based upon the reactivity of this steroid with an antiserum induced by the 3-carboxymethyloxime of 18, 21-aldosterone diacetate conjugated with bovine serum albumin. One hundred microliters of urine enzymatically hydrolyzed with an helix pomatia preparation, containing tritiated tetrahydroaldosterone for the yield calculation, were extracted with dichloromethane and chromatographed on a small celite column. The yield after extraction and chromatography was 64 +/- 17%. The radioimmunological determination was carried out in a conventional manner. The method is specific, sensitive (10 pg/tube), exact, reproducible, very simple and extremely rapid. The results showed good agreement with values given by a colorimetric method (p less than 0.001). The median value measured in 45 healthy adult subjects under standard sodium diet was 53.3 microgram/24h (95 % of the population within a 16.6 to 131.1 microgram/24h range). In 78 cases of adrenocortical insufficiency, 60 cases of obesity and 28 cases of hypokalemia, the median values (and the ranges : microgram/24h) were respectively 7.7 (1.0 - 51.0), 80.9 (17.0 - 503.0) and 64.3 (8.0 - 181.0). In 330 hypertensive patients the excretion of tetrahydroaldosterone exceeded the normal range in 115 cases (35%) with a median of 199.7 microgram/24h (131 to 620 microgram/24h).
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PMID:Radioimmunological determination of urinary tetrahydroaldosterone. 91 Feb 48

High blood pressure of unknown etiology has been related to many pathogenetic factors, mainly dietary salt intake, mental stress, alcohol consumption, sedentary living and aging. Hypertension is more common in condition such as obesity and diabetes mellitus. Sustained elevation of arterial pressure is mediated by vasoconstriction in response to catecholamine release and activation of the renin-angiotensin-aldosterone system. In obese and diabetic subjects, insulin resistance and hyperinsulinemia have been found to be related to development of hypertension. The hypertension phenotype may correspond to many different genotypes codifying various alterations of hormone and receptor function, as well as inherited diseases linked to hypertension. An outstanding epidemiologic example of how hypertension may appear in a community is found in Easter Island. Hypertension among native adults increased from 3 to 30% in a 10 year period, in relation to influx of tourism and changes in salt intake and diet.
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PMID:[Etiopathogenic factors of arterial hypertension]. 134

Sodium excretion and the blood levels of aldosterone, renin, atrial natriuretic peptide (ANP), and insulin were investigated in 9 women with obesity of alimentary-constitutional type during hunger therapy and resumed nutrition. It has been assumed that restricted sodium excretion with the kidneys during fasting is mainly caused by activation of the renin-angiotensin-aldosterone system, with ANP contributing to it, insulin not playing the major role in this process.
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PMID:[Hormonal regulation of sodium excretion by the kidneys during hunger therapy of obese patients]. 138 80

The incidence of hypertension is increased in obesity, a state associated with an insulin resistance syndrome. By using an euglycemic clamp method, Ferrannini et al. demonstrated the existence of an insulin resistance state in patients with essential hypertension. However, the body mass index of the subjects studied appeared to be slightly excessive. This abnormality has not been observed in patients with secondary hypertension. Insulin resistance is probably localized to peripheral tissues such as muscles and may be associated with other cellular abnormalities. Can insulin resistance, characterized by a raised circulating insulin concentration in the presence of normal blood glucose, be responsible for certain "modifications" associated with essential hypertension? Insulin induces sodium retention and increases the aldosterone-secreting effect of angiotensin II. These effects are likely to promote a rise in blood pressure and an increase in the sensitivity of vessels to endogenous substances. Moreover, insulin is a known growth factor and is involved in lipoprotein metabolism. If insulin resistance plays an important role in the maintenance of complications of essential hypertension, it is important that the treatments used tend to correct this anomaly. Thiazide diuretics and beta-blockers aggravate insulin resistance while angiotensin converting-enzyme inhibitors correct this condition.
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PMID:[Arterial hypertension, hyperinsulinism and insulin resistance]. 143

Prolactin and aldosterone secretion and renin activity in the plasma were measured in the course of thyroliberin (TRH) test in women with various endocrine diseases, both connected with the water-salt metabolism disturbances and without these--with the idiopathic edemas (n = 11), hypothyrosis (n = 16), Stein-Leventhal'syndrome (n = 6), and obesity (n = 8). A reciprocal relationship between prolactin concentrations (a drastic elevation) and aldosterone levels (lowered) were revealed, as were universal responses of both the hormones to TRH administration in patients with various conditions. The authors come to a conclusion on the absence of a stimulating effect of prolactin on aldosterone secretion and plasma renin activity. They suggest an indirect contribution of prolactin to the regulation of the renin-aldosterone system, probably via dopaminergic mechanisms.
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PMID:[Interrelationships between prolactin and the renin-aldosterone system in patients with various endocrine diseases]. 148 May 91

Impairment of glucose and lipid metabolism is common in hypertensive subjects. In the present study the relationships between indices of lipid and glucose metabolism and the renin-aldosterone system were studied in 37 untreated hypertensive subjects (DBP greater than 95 mmHg). Fasting insulin and the early insulin response at an intravenous glucose tolerance test were both correlated to plasma renin activity (r = 0.48, P less than 0.003 and r = 0.55, P less than 0.002, respectively) while HDL-cholesterol was found to be inversely related to the urinary excretion of aldosterone (r = 0.35, P less than 0.03). These relations were still significant when influences of age, sex, obesity (BMI) and serum creatinine were taken into account in the multiple regression analysis. In conclusion, hyperinsulinaemia and low levels of HDL-cholesterol were found in hypertensive subjects with a high activity of the renin-aldosterone system and might explain the high incidence of cardiovascular diseases found in this group.
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PMID:Metabolic cardiovascular risk factors and the renin-aldosterone system in essential hypertension. 158 27


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