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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the role of sodium intake in the regulation of blood pressure in obese subjects, we measured blood pressure in 60 obese and 18 nonobese adolescents after successive two-week periods of a high-salt diet (greater than 250 mmol of sodium per day) and a low-salt diet (less than 30 mmol per day). When they were changed from a high-salt to a low-salt diet, the obese group had a significantly larger mean change (+/- SE) in mean arterial pressure (-12 +/- 1 mm Hg) than did the nonobese group (+1 +/- 2 mm Hg; P less than 0.001). The variables that best predicted the degree of sodium sensitivity were the fasting plasma insulin level, the plasma aldosterone level while the low-salt diet was being given, the plasma norepinephrine level while the high-salt diet was being given, and the percentage of body weight made up by fat. Fifty-one of the obese adolescents were also studied before and after a 20-week weight-loss program. After the weight-loss program, the 36 subjects who lost more than 1 kg of body weight had a reduced sensitivity of blood pressure to sodium (difference from value during high-salt diet to that during low-salt diet, -1 +/- 1 mm Hg). The blood pressure of the remaining 15 adolescents was still sensitive to sodium intake (-11 +/- 3 mm Hg). These results support the hypothesis that the blood pressure of obese adolescents is sensitive to dietary sodium intake and that this sensitivity may be due to the combined effects of the hyperinsulinemia, hyperaldosteronism, and increased activity of the sympathetic nervous system that are characteristic of obesity.
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PMID:The effect of weight loss on the sensitivity of blood pressure to sodium in obese adolescents. 230 Jan 15

To determine the impact of the renin-angiotensin-aldosterone system on left ventricular function and structure, 36 untreated patients with essential hypertension (WHO class I and II) were examined. Posterior wall thickness, relative wall thickness, and left ventricular mass were determined by M-mode echocardiography. Plasma renin activity, aldosterone, angiotensin I, and angiotensin II levels were measured by radioimmunoassay. Plasma renin activity was related to 24-hour urinary sodium excretion. Of all the endocrine parameters, only the angiotensin II level correlated with posterior wall thickness (r = 0.50, p less than 0.05) and relative wall thickness (r = 0.46, p less than 0.05). This relationship was confirmed by stepwise multiple regression analysis taking arterial pressure, obesity, and sodium excretion into account (p less than 0.05). Plasma renin activity but not the angiotensin II level correlated positively with the ejection fraction (r = 0.42, p less than 0.05) and velocity of circumferential fiber shortening (r = 0.57, p less than 0.01). Thus, angiotensin II emerged as a determinant of left ventricular structural adaptation in essential hypertension.
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PMID:Does the renin-angiotensin-aldosterone system modify cardiac structure and function in essential hypertension? 297 63

Data from several epidemiologic studies have suggested that the prevalence of hypertension in patients with diabetes mellitus is approximately 1.5-2.0 times greater than in an appropriately matched nondiabetic population. In patients with insulin-dependent diabetes mellitus (IDDM), hypertension is generally not present at the time of diagnosis. As renal insufficiency develops, blood pressure rises and may exacerbate the progression to end-stage renal failure. In non-insulin-dependent diabetes mellitus (NIDDM), many patients are hypertensive at the time of diagnosis. The incidence of hypertension in NIDDM is related to the degree of obesity, advanced age, and extensive atherosclerosis that is typically present, and it probably includes many patients with essential hypertension. Several other pathophysiologic mechanisms also contribute to the genesis and maintenance of hypertension in the patient with diabetes. Hyperglycemia and increases in total-body exchangeable sodium may lead to extracellular fluid accumulation and expansion of the plasma volume. In some patients, alterations in the function of the renin-angiotensin-aldosterone system and vascular sensitivity to vasoactive hormones may also play a role. It has recently been suggested that hyperinsulinemia and insulin resistance may also contribute to the maintenance of an elevated blood pressure because insulin is known to promote sodium retention and enhance sympathetic nervous system activity. The evidence for these hypotheses and their respective contributions to the etiology of hypertension in IDDM and NIDDM are discussed.
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PMID:Etiology and prevalence of hypertension in diabetic patients. 307 72

We conclude that the following may explain the rise in blood pressure with obesity and the subsequent fall in blood pressure (Fig. 2): (1) An increase in calories, protein, or carbohydrate leads to an increase in plasma catecholamines, sympathetic nervous system activity, and insulin secretion. (2) These factors, in turn, lead to increased renal sodium retention and stimulation of the renin-aldosterone system which, in turn, leads to: (3) An increased cardiac output with an inability to appropriately adjust the peripheral resistance to maintain normotension with resultant hypertension. Conversely, the fall in blood pressure with weight reduction can be explained by (Fig. 3): (1) A decrease in calorie, carbohydrate, or protein intake which leads to: (2) A decrease in circulating plasma catecholamines, sympathetic nervous system activity, and insulin secretion which results in: (3) A natriuresis and decrease in the renin-aldosterone system, which causes a decrease in circulating blood volume and in cardiac output. This, in turn, lowers blood pressure towards normal. The unanswered question still remains: why do some obese patients become hypertensive and others remain normotensive? Perhaps there are weight-sensitive individuals and weight-resistant individuals just as there appear to be salt-sensitive and salt-resistant hypertensive patients. Perhaps the answer is genetic. These questions also remain to be answered.
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PMID:Mechanisms of hypertension in obesity. 332 17

The long-term results of surgical and specific drug therapy were compared in a group of 57 patients with primary aldosteronism (PA) (46 with aldosterone-producing adenoma (APA), 11 with idiopathic hyperaldosteronism (IHA) and bilateral adrenal hyperplasia). Unilateral adrenalectomy completely normalized blood pressure (BP) in 77.1% of surgically treated APA, evidently improving hypertension in remaining 22.9%. No recurrence of the adenoma in the remaining adrenal was seen in any of the surgical APA cases. In 19 of the non-surgical patients (11 with APA, 8 with IHA) monotherapy with spironolactone reduced blood pressure in 73%, though total BP normalization was an exception. The treatment normalized hypokalemia, low total exchangeable potassium, tendency to hypernatremia, and high total exchangeable sodium. Surgical as well as conservative therapy increased to normal or above-normal levels plasma renin activity suppressed prior to treatment. Pre-operatively high urine and plasma aldosterone levels normalized in all adrenalectomized patients, but remained above the normal range during spironolactone therapy in spite of a small decline in its absolute values. The disturbances of maximum renal concentrating capacity due to impaired nephron responsiveness to sufficiently high endogenous vasopressin concentrations were completely eliminated after kaliopenic nephropathy had been repaired. The other renal functions remained within normal values. Echocardiographically diagnosed left ventricular hypertrophy was seen less often than in the other types of arterial hypertension, tending to regress after APA management. Our longitudinal study (2-16 years) showed primary aldosteronism as a well curable, albeit rare, cause of hypertension. As regards BP and laboratory tests normalization, better results were achieved in surgical APA cases than in patients treated with spironolactone. Older age, longer history of hypertension and more frequent incidence of obesity, nephrosclerosis and pyelonephritis may be responsible for hypertension persisting after surgical treatment.
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PMID:Long-term results of surgical and conservative treatment of patients with primary aldosteronism. 345 May 33

To determine the role of aldosterone in the regulation of blood pressure (BP) in obese adolescents, supine and 2-hour upright plasma renin activity (PRA), and aldosterone and cortisol were measured in 10 nonobese and 30 obese adolescents before and after a 20-week weight loss program. The obese adolescents had significantly higher supine and 2-hour upright plasma aldosterone concentrations (17 +/- 8 vs 6 +/- 2 ng/dl [p less than 0.01 supine obese vs nonobese] and 30 +/- 11 vs 14 +/- 8 ng/dl [p less than 0.01 2-hour upright]). Although PRA was not significantly different between the 2 groups of children, a given increment in PRA produced a greater increment in aldosterone in the obese adolescents. In addition, obese subjects had a significantly increased mean BP (93 +/- 12 vs 74 +/- 8, p less than 0.005) and a weak correlation between BP and plasma aldosterone concentration. Compared with an obese control group, weight loss resulted in a significant decrease in plasma aldosterone (p less than 0.01) without an associated decrease in PRA. After weight loss there was also a significant decrease in the slope of the posture-induced relation between PRA and aldosterone. In addition to weight loss being associated with a significant decrease in BP (p less than 0.01), there was a significant correlation between the change in plasma aldosterone and the change in mean BP (r = 0.538; p less than 0.002 change in upright aldosterone vs change in mean BP). Obese adolescents have an increased plasma aldosterone concentration that may be important in the regulation of their BP.
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PMID:Role for aldosterone in blood pressure regulation of obese adolescents. 351 21

According to textbooks, Cushing's syndrome (CS) is associated with a loss of the circadian rhythmicity in circulating cortisol. Documented cases of a persisting rhythm in CS are regarded as an exception. Herein, we show that a circadian rhythmicity in plasma cortisol, albeit of much reduced amplitude and with altered timing, remains a group characteristic of patients with CS, characterized further by a circadian rhythm in circulating aldosterone. In Lubochna, Czechoslovakia, 28 patients with CS, 120 patients with obesity imitating CS, 70 subjects with simple obesity, and 19 nonobese controls were sampled at 0800, 1600, 2000, 0000, and again at 0800 on the following day. In Rome, five women and three men with CS and 27 women and 30 men in clinical health gave blood for aldosterone determinations at 0600, 0800, 1200, 1800, 2000, and 0000. Results were first analyzed by single cosinor and then summarized by population-mean cosinor. A group rhythm was demonstrated for all categories of subjects by the methods employed, although, compared to health and even to simple obesity or Cushing-imitating obesity, the amplitude of the rhythm in CS was much reduced. Subgrouping according to etiology and individualized assessment in practice are mandatory. The scope of this group rhythm assessment, however, is merely to document that as a general rule the circadian rhythms in circulating cortisol and aldosterone persist in CS documented by surgery or at autopsy.
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PMID:Altered circadian plasma cortisol and aldosterone group rhythms in Cushing's syndrome versus obesity and health. 362 33

Ten patients with hypertension and obesity were studied during a program of weight loss on an unrestricted sodium diet. The study showed that weight loss during the ten month period was accompanied by a significant decrease in urinary aldosterone, tetrahydroaldosterone -3-glucuronide and plasma renin activity values. It was also demonstrated that successful reduction in body weight was associated with a reduction in blood pressure. It is postulated that blood pressure reduction in obese patients during weight reduction may depend on decreases in aldosterone and plasma renin activity. The reduction in levels of tetrahydroaldosterone-3-glucuronide is due to an energy related depression of the glucuronidation process caused by carbohydrate deficiency. It is postulated that the lowered rate of metabolism of aldosterone as measured by the diminished formation of the metabolite tetrahydroaldosterone-3-glucuronide is an important determinant of blood pressure status during weight reduction.
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PMID:Aldosterone studies in obese patients with hypertension. 389 May 39

Pubertal juvenile dyspituitarism (PJD) is one of the common types of obesity in adolescents. Literature data on the involvement of the renin-angiotensin-aldosterone, hypophysis-adrenal cortex system in the formation of this syndrome are of controversial nature, and the pathogenesis of the development of arterial hypertension in PJD is obscure in many respects. The purpose of the study was to investigate the activity of plasma renin, potassium and sodium in the blood serum as well as the excretion of potassium and sodium with daily urine in PJD patients. A total of 148 PJD patients aged 14 to 21 were examined, of them 22 had exogenous constitutional obesity. The control group was composed of 54 healthy persons of the same sex and age. Electrolyte metabolic derangement, an increase in the ACTH level and hyperaldosteronemia were shown to play a certain role in the development of arterial hypertension in PJD. The above changes developed in the presence of disordered interrelationships in the hypophysis-adrenal cortex, renin-angiotensin-aldosterone system.
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PMID:[Pathogenesis of arterial hypertension in puberal juvenile dyspituitarism]. 390 40

A study was made of change in hormone secretion in 243 patients with alimentary-constitutional and hypothalamic obesity. Activation of the somatostatin mechanism, a decrease in somatotropic and thyrotropic function of the hypophysis, an increment of corticotropin, beta-lipotropin and vasopressin levels in the blood, disturbance of circadian fluctuations of hormone secretion, an increase in insulin and C-peptide secretion, a decrease in glucagon secretion and triiodothyronine and cortisol levels in the blood, activation of the renin-aldosterone system and cortisol secretion rate were equally expressed both in alimentary-constitutional and primary hypothalamic obesity. The central mechanisms of the regulation of endocrine functions were incorporated in a pathological process even in alimentary-constitutional obesity. Disorders of the hypothalamic regulation lay in the basis of both types of obesity.
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PMID:[Comparative evaluation of the hormonal changes in alimentaro-constitutional and hypothalamic obesity]. 395 72


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