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

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

We studied nocturnal and early morning variations in the concentration of plasma atrial natriuretic peptide (ANP) in 17 men who habitually snored. The subjects had a mean age of 51.0 +/- 5.8 years, range 41-62 y with a mean body mass index (BMI) of 32.9 +/- 7.3 kg/m2. The concentration of plasma ANP was measured by radioimmunoassay of venous samples at 10 p.m., midnight, 6 p.m. and 8 p.m. All night sleep recordings were conducted with the static charge sensitive bed to monitor body and breathing movements and a BIOX III Pulse Oximeter for the blood oxygen saturation level. Nine patients were defined as having the obstructive sleep apnea syndrome (OSAS). No significant diurnal variation for ANP concentrations was detected. At 8 a.m. five OSAS patients and two others had ANP concentrations above normal (70 pg/ml). Neither mean oxygen saturation during the night nor arterial hypertension discriminated between the high and low ANP groups at 8 a.m. The best discriminators for a high concentration of ANP at 8 p.m. were marked obesity (BMI greater than or equal to 30 kg/m2), over 400 movements lasting less than five seconds, and over 30% of active sleep per night. In a multivariate regression analysis age, percentage of active sleep during the night, BMI and the median oxygen saturation level during the night explained 76.4% of the total variance of ANP at 8 a.m. In a similar analysis the median oxygen saturation level during the night and BMI both explained the variance of ANP significantly. The whole model explained 53.7% of the variance of the ANP concentrations at 6 a.m.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic peptide in habitual snorers. 182 3

The purpose of this study was to determine if the reflex response to a saline load is altered in the obese Zucker rat. The obese Zucker rat is a genetic model of obesity and insulin-resistant diabetes that has been reported to have high blood pressure. We examined the reflux renal responses to volume expansion in both anesthetized obese and lean Zucker rats. Initial blood pressure was significantly elevated in the obese Zucker rats compared with the lean controls. Urine flow and sodium excretion from innervated and denervated kidneys were measured before and after volume expansion with normal saline. Volume expansion resulted in significantly less urine flow and sodium excretion in the obese than the lean Zucker rats. This response was evident in both the intact and denervated kidneys. Rats were then infused with atrial natriuretic peptide (ANP) to determine if natriuretic and diuretic responses were altered in these rats. The diuretic action of ANP was not significantly reduced in the obese Zucker rat. However, the natriuretic action of ANP was significantly attenuated in the obese rats. These results indicate that the reflux response to an acute saline load is attenuated in the obese Zucker rat and that this decreased response may be due to a reduction in the direct action of ANP on the kidney.
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PMID:Reduced renal responses to an acute saline load in obese Zucker rats. 183 69

Renal clearance studies were conducted in conscious, chronically catheterized obese and lean Zucker rats to investigate the natriuretic responses to i) acute IV infusion of isotonic NaCl = 5% of total body weight and ii) IV infusion of alpha rat atrial natriuretic peptide (ANP) in a dose of 300 ng/kg/min. In the baseline state, arterial blood pressure (BP) was significantly higher in obese vs lean rats. Absolute values of GFR and sodium excretion were similar but lower in obese vs lean rats when factored for body weight. In the 2 h period during and after NaCl infusion, obese rats showed a greater natriuresis vs lean while BP rose significantly and similarly. ANP infusion was natriuretic in obese rats but had no effect on lean rats. ANP lowered BP in both groups but BP remained higher in obese vs lean rats at all times. These studies show that in the chronic, unstressed preparation the 6-8 month old, female Zucker obese rat has a higher BP vs the 6-8 month old lean Zucker. The short term natriuretic response to either a NaCl load or ANP infusion is greater in obese vs lean Zuckers and the depressor response to ANP is intact in obese Zuckers. Thus the higher BP in this model of obesity is unlikely to be due to either a defective response to ANP or to a defect in the renal response to acute sodium challenge.
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PMID:Short term natriuretic responses in the conscious Zucker obese rat. 183 82

Epidemiological evidence suggests that there is a close association between obesity, non-insulin-dependent diabetes (NIDDM) and hypertension. Obesity and NIDDM are the classical insulin-resistant states. Even in the absence of these conditions, essential hypertension is associated with insulin resistance. In view of the acute effects of insulin on renal sodium reabsorption, the sympathetic nervous system, the renin-angiotensin-aldosterone system, the transmembranous cation transport, the cardiovascular reactivity, the atrial natriuretic peptide and the kallikrein-kinin system, hyperinsulinaemia may contribute to the development of hypertension in these diseases. Preliminary evidence suggests that sensitivity to these possible blood-pressure-elevating action(s) of insulin is still present despite the resistance to the glucose-lowering action of the hormone. However, extrapolation of the epidemiological data and results of acute experiments indicate that the impact on blood pressure is rather small. The pathophysiological mechanisms of hypertension in the above-mentioned conditions are also not always consistent with insulin action(s). Moreover, some data suggest that insulin resistance, and not hyperinsulinaemia per se, underlies the blood pressure elevation, while the possibility cannot be excluded that both hypertension and insulin resistance are co-inherited, but unrelated, abnormalities.
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PMID:Insulin and blood pressure regulation. 204 23

Obesity is usually associated with expansion of blood volume. Therefore, we studied whether obesity affects cardiac and plasma atrial natriuretic peptide (ANP) levels in experimental animal model. Mice made obese with gold thioglucose developed cardiac hypertrophy associated with increases in ANP in atrial tissue and plasma. There were significant (p less than 0.01) correlations between the cardiac ANP concentration and body weight or cardiac weight. These data suggest that enhanced synthesis of atrial ANP in obese mice can be mainly ascribed to increased blood volume associated with cardiac hypertrophy.
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PMID:Cardiac atrial natriuretic peptide concentrations in experimental obese mice. 215 Aug 10

The effect of obesity and weight reduction upon circulating concentrations of atrial natriuretic peptide was assessed in an experimental model of the disease. Obese rats weighing in excess of 750 g were compared with formerly obese animals subjected to a 15-week period of caloric restriction resulting in a 40% reduction in body weight. Mean adipocyte size was significantly reduced with weight loss, as was estimated body fat. Mean arterial blood pressure remained normotensive for both groups, but a significant reduction in heart rate was associated with weight reduction. Circulating atrial natriuretic peptide was significantly elevated in the lean rats, which also exhibited decreased plasma renin activity and a negative sodium balance. Analysis of heart to body weight ratios implied that an obesity-associated, volume-induced cardiac hypertrophy remained even after the normalization of body fat. These results suggest that the diuresis and natriuresis accompanying weight reduction may be facilitated by atrial natriuretic peptide, which was elevated in part due to a persistent left ventricular hypertrophy following the transition from the obese to lean condition.
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PMID:Effect of experimental obesity and subsequent weight reduction upon circulating atrial natriuretic peptide. 252 48

Epidemiologic studies suggest a close association between hypertension, obesity, and diabetes. It has been demonstrated that essential hypertension, per se, is an insulin-resistant state. However, the pathogenesis of the association between insulin resistance and hypertension is poorly understood. Elevated plasma insulin levels may contribute to the development of hypertension through renal sodium reabsorption, the sympathetic nervous system, the transmembranous cation transport, the renin-angiotensin system, the cardiovascular reactivity, and the atrial natriuretic peptide. Diuretics, beta-blockers, calcium antagonists, angiotensin-converting enzyme (ACE) inhibitors, and alpha 1-antagonists are first-choice drugs in the management of hypertension. Diuretics, except indapamide, impair insulin sensitivity and glucose tolerance. The same negative effects, exerted by beta-blockers, are reduced employing those with selective activity. With few exceptions, calcium antagonists have no adverse influence on carbohydrate metabolism. ACE inhibitors and alpha 1-antagonists do not influence or even improve glucose metabolism.
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PMID:Carbohydrate metabolism in hypertension: influence of treatment. 750 68

Plasma atrial natriuretic peptide (ANP) concentrations were determined in basal conditions and after infusion of 1000 ml of 0.9% NaCl in women with anorexia nervosa, in normotensive obese women and in healthy women of the control group. Additionally, in the obese women and in the controls, plasma ANP was measured after iv injection of clonidine. Anorectic patients were investigated in the period of weight loss (mean deficit of body weight was 40%). The mean body mass index (BMI) in the obese women was 36.44 +/- 0.36 kg/m2. Basal plasma ANP concentrations were significantly higher in both anorectic and obese women (p < 0.001 and p < 0.01, respectively). The response of ANP to acute water load was markedly blunted in anorexia nervosa and in obesity (delta % = 232% in control group, 14% in anorexia nervosa and 21% in obesity. A significant increase of ANP was found after iv injection of clonidine in the control group and in obesity (p < 0.001 and p < 0.01, respectively). However, the increase of response (expressed as a percentage change) in obese patients was lower than that in the control group (delta % = 64% and 199%, respectively). The response of ANP to alpha 2-adrenergic stimulation was higher than to hemodynamic stimulus. Our results suggest that the disturbed control of neuropeptides and neurotransmitters as well as changes in peripheral metabolism may explain the impaired responsibility of ANP to hemodynamic stimuli in anorectic and obese patients.
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PMID:Impaired response of atrial natriuretic peptide to acute water load in obesity and in anorexia nervosa. 924 7

Measurements of blood lipids and hormones (plasma renin, aldosterone, vasopressin, prolactin, atrial natriuretic peptide, beta-endorphin, thyrotropin, thyroid hormones) in two groups of patients suffering from obesity (group 1: 64 patients with arterial hypertension and group 2: 26 patients with normal arterial pressure) have brought the authors to a conclusion that arterial hypertension in young obese patients is an early manifestation of essential hypertension. Hormonal dysfunction in obese patients is conducive to early development of essential hypertension in cases when there is a hereditary predisposition to it.
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PMID:[Hormonal aspects of the pathogenesis of arterial hypertension in young obese patients]. 810 42


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