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

Hypertension is the commonest cardiovascular disease in Africans occurring in more than 15% of the adult population in some studies. It occurs in the lower as much as in the higher socio-economic groups. Recent studies have confirmed earlier findings that essential hypertension in Africans is characterised by volume loading, low plasma renin activity, high salt taste threshold, high urinary sodium and low potassium excretion and high plasma aldosterone. The commonest complication of hypertension in Africans is congestive cardiac failure followed by cerebrovascular accidents. Coronary heart disease is rare. Even in the absence of overt heart failure and compounding factors like obesity, alcoholism, cigarette smoking, diabetes mellitus and myocarditis, evidence of abnormal left ventricular morphology and function is often present in newly diagnosed patients with moderate or severe hypertension. Response to monotherapy with beta-blockers or ACE inhibitors is usually poor but is good with thiazide diuretics or calcium channel blockers. The diuretics are an essential component of a two or three drug regime containing other classes of antihypertensive drugs. Cost of drugs is the most important determinant of compliance with drug treatment and consequently the likelihood of progression of the diseases to more severe forms in long term follow-up.
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PMID:Hypertension in Africa and effectiveness of its management with various classes of antihypertensive drugs and in different socio-economic and cultural environments. 826 3

Obesity is considered to be a major factor in the pathogenesis of hypertension in industrialized countries. Recent studies have suggested that the kidneys may play an important role in the development of obesity-induced hypertension. The purpose of this study was to determine whether obesity-induced hypertension is associated with abnormalities in the pressure-natriuresis relation. Renal function studies were performed in anesthetized control dogs (body weight, 20.2 +/- 0.8 kg) and obese dogs (body weight, 26.4 +/- 0.7 kg) that were maintained on a high-fat diet for 5 to 6 weeks. Mean arterial pressure averaged 122 +/- 5 mm Hg in the control group (n = 6) and 148 +/- 7 mm Hg in the obese group (n = 8). The effects of renal perfusion pressure on renal hemodynamics as well as sodium and water excretions were examined at five levels of renal perfusion pressure ranging from 75 to 165 mm Hg. Pressure-natriuretic and diuretic responses were reduced in the obese dogs by 40% to 50%. The renal blood flow and glomerular filtration rate autoregulatory responses and fractional lithium excretion responses to changes in renal perfusion pressure were similar in the control and obese dog groups. Associated with the attenuated natriuretic response to renal perfusion pressure in the obese dogs were significant elevations in plasma renin activity (4.3 +/- 1.6 versus 1.6 +/- 0.5 ng angiotensin I/mL per hour), plasma aldosterone concentration (34.4 +/- 6.4 versus 15.3 +/- 3.2 ng/dL), and plasma insulin concentration (30.5 +/- 6.8 versus 20.9 +/- 2.9 IU/mL).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal pressure natriuresis in the dog model of obesity-induced hypertension. 828 80

The arteriosclerotic diseases and their risk factors were retrospectively investigated in 44 patients with chronic state of acute carbon monoxide intoxication who had been admitted since November 1963. The lack of elevations of systolic and diastolic blood pressure, serum cholesterol, fasting blood glucose and obesity index with advancing age was shown in these patients. During the observation period (mean 23.3 years), cardiovascular diseases developed in three patients, (brain hemorrhage, brain infarction, and myocardial infarction in each) but none of the patients died from such diseases. Therefore, the morbidity and mortality of arteriosclerotic diseases were less frequent than those reported in the community population. This observation seems to be attributable to the dietary and environmental control of risk factors during the long-term hospitalization. On the other hand, total protein, hematocrit, cardiothoracic ratio and calcification of the aorta on the chest X-ray, echocardiographic findings, plasma renin activity and plasma aldosterone concentration at the final examination in 1993 were similar to those seen in the community population. These findings indicate that long-term control of risk factors by hospitalization results in the lack of blood pressure increase with age and less prevalence of arteriosclerotic diseases.
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PMID:[Study on serial changes in blood pressure, obesity and blood chemistry and cardiovascular disease in the long-term hospitalized patients with sequela of acute carbon monoxide poisoning]. 858 58

To access the role of insulin resistance in obesity hypertension, we examined the change of insulin sensitivity after weight loss in 24 obese hypertensive subjects by the euglycemic hyperinsulinemic glucose clamp method. The results of the 4-week calorie-restricted diet were a weight loss of 10.2% (from 74 +/- 12 to 67 +/- 11 kg, P < .01) and a decrease in mean blood pressure of 13.1% (from 124 +/- 7 to 107 +/- 9 mm Hg, P < .01). A decrease in plasma norepinephrine (from 208 +/- 74 to 142 +/- 52 pg/mL, P < .01) was associated with decreases in plasma renin activity (from 1.06 +/- 0.98 to 0.62 +/- 0.63 ng/mL per hour, P < .01) and serum aldosterone (from 70 +/- 28 to 57 +/- 24 pg/mL, P < .05). Glucose infusion rate increased significantly (42.9%), from 809 +/- to 1155 +/- 251 mumol/m2 per minute. The insulin sensitivity index, which is a measure of the glucose infusion rate divided by plasma insulin, increased significantly (42.6%), from 10.8 +/- 3.5 to 15.4 +/- 4.4 (mumol/m2 per minute)/(microU/mL). Stepwise multiple linear regression analysis showed that changes of plasma norepinephrine, insulin sensitivity index, plasma renin activity, and age were significant predictive factors for the change of mean blood pressure after weight loss. These results indicate a distinct relation between an improvement of insulin sensitivity and a decrease in blood pressure after weight loss in obese hypertensive subjects. The decrease in blood pressure after weight loss is probably related to the suppression of sympathetic nervous activity.
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PMID:Improvement of insulin sensitivity contributes to blood pressure reduction after weight loss in hypertensive subjects with obesity. 862 Dec 14

1. In the present study, using the euglycaemic hyperinsulinaemic glucose clamp technique, we investigated the effects of hyperinsulinaemia on sodium-water metabolism and the pressor system in obesity, both of which have been reported to be closely associated with insulin resistance and/or hyperinsulinaemia. 2. Sixteen obese young subjects and 24 non-obese young subjects who were all normotensives, participated in this study. The 2 h euglycaemic hyperinsulinaemic glucose clamp was performed in a fasting state. The mean glucose infusion rate needed to maintain a fasting blood sugar level (FBS) during the last 30 min of the clamp was used as an indicator of insulin sensitivity (M-value). Before and after the clamp, the following parameters were measured: creatinine clearance (Ccr); urinary excretion of sodium (UNaV); fractional excretion of sodium (FENa); plasma renin activity (PRA); plasma aldosterone concentration (PAC) and plasma noradrenaline concentration (PNA). 3. The M-value was significantly lower in obese subjects compared with non-obese subjects, although FBS and fasting immunoreactive insulin levels were similar in both groups. UNaV and FENa fell only in obese subjects during the clamp, while Ccr showed no significant change in either group. PNA and PRA increased significantly and PAC tended to increase in both groups. 4. These results suggest that obese subjects have insulin resistance with respect to glucose metabolism, but that urinary sodium excretion and the pressor system remain insulin-sensitive; the sensitivity of the sodium retaining action to hyperinsulinaemia was actually higher in obese subjects than in non-obese subjects. Therefore, if compensatory endogenous hyperinsulinaemia was raised by insulin resistance, these two factors may lead to chronic sodium retention and pressor system stimulation and, in turn, to hypertension in obesity.
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PMID:Effects of hyperinsulinaemia on renal function and the pressor system in insulin-resistant obese adolescents. 871 63

Obesity is associated with risk-factor clustering, including risk factors for hypertension, hyperinsulinemia, resistance to insulin's lowering of glucose and fatty acid concentrations, and a complex dyslipidemia. Obese hypertensive subjects are presumed to be salt sensitive because of the antinatriuretic actions of insulin. However, in our studies obese hypertensive subjects aged < 45 y were not more salt sensitive than were lean individuals. Subjects with the greatest evidence for risk-factor clustering had higher renin and aldosterone concentrations, which increased with salt restriction. The greater rise of fatty acids and activation of the renin-angiotensin system may explain the larger elevations of blood pressure, insulin, and triacylglycerol with salt restriction in high-risk subjects than in low-risk subjects. Regardless of mechanism, the adverse effects of short-term, very-low-salt diets in high-risk subjects suggest that continued moderation in advice for universal salt restriction is appropriate.
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PMID:Adverse effects of short-term, very-low-salt diets in subjects with risk-factor clustering. 902 63

This paper approaches the hypothesis that fatty acids contribute to hypertension by examining possible interactions of nonesterified fatty acids with renal pressure-natriuresis, peripheral vascular resistance, and the central nervous barostat, three loci where long-term regulation of blood pressure is probably controlled. By inhibiting aldosterone secretion, nonesterified fatty acids may lower blood pressure by facilitating pressure-natriuresis. Oxygenated metabolites of fatty acids appear to stimulate aldosterone secretion. In different experimental situations, fatty acids either constrict or dilate arteries. There is no evidence of an effect of fatty acids on the central nervous barostat, but they do sensitize peripheral vessels to alpha-adrenergic stimuli. Obesity and diabetes are marked by increased incidence of hypertension, and elevated levels of fatty acids or their P450 oxygenated metabolites may contribute to this association. Drugs that influence plasma fatty acids, like heparin, do not have reproducible effects on blood pressure. Experimental evidence suggests but does not prove that nonesterified fatty acids can affect the long-term set-point of blood pressure.
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PMID:Nonesterified fatty acids in the pathogenesis of hypertension: theory and evidence. 925 Jun 9

We have investigated the possible involvement of endogenous corticosteroids in the maintenance of hypertension in aged lean and obese Zucker rats using the type II corticosteroid antagonist mifepristone. At 8 mo of age, the start of the study, obese Zuckers had been hypertensive for at least 2 mo (systolic blood pressure; 153 +/- 4 vs. 136 +/- 5 mmHg; n = 8-9; P < .05) and were hyperinsulinemic (756 +/- 98 vs. 193 +/- 61 microU x ml(-1)) and hypercorticosteronemic (524 +/- 83 vs. 260 +/- 97 ng x ml(-1)) compared to their lean littermates. There were no differences in plasma renin activity between lean and obese animals and plasma renin activity was unaffected by any treatment. Oral treatment of obese rats with mifepristone (40.0 mg x kg(-1) day(-1) for 9 days) resulted in a gradual reduction in SBP to lean levels by day 9. Mifepristone treatment did not affect plasma insulin or corticosterone levels but resulted in a significant reduction in plasma aldosterone concentration. Mifepristone was without significant effect on systolic blood pressure in lean rats. Oral treatment of lean rats with corticosterone-21-acetate (3.0 mg x kg(-1) day(-1) for 9 days) resulted in a rise in systolic blood pressure to levels similar to obese Zuckers after 9 days. Plasma insulin levels were unchanged but corticosterone immunoreactivity was significantly reduced. Plasma aldosterone levels were increased from 564 +/- 3 to 802 +/- 68 pg x ml(-1). Our data suggest that raised glucocorticoids and aldosterone may be factors contributing to hypertension in obesity.
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PMID:Effects of the glucocorticoid II receptor antagonist mifepristone on hypertension in the obese Zucker rat. 931 65

For the purpose of understanding the antiobesity effect of acupuncture and it's influence on water and salt metabolism in the patients suffering from simple obesity, we have observed the changes of symptoms and signs, obesity indices, blood sodium, blood potassium, mOsm of plasma and urinary aldosterone before and after acupuncture treatment in 75 patients with simple obesity (12 cases with edema, 33 cases without edema). The results showed that the total effective rate of antiobesity treatment for one month was 89.3%. Before acupuncture the concentrations of blood sodium and aldosterone of the patients with edema were significantly higher than those of normal persons or the patients without edema, but the concentration of blood potassium and mOsm of plasma of the patients with edema were significantly lower than those of normal persons or the patients without edema. After acupuncture treatment the concentrations of blood sodium and aldosterone decreased markedly and the concentration of blood potassium and mOsm of plasma increased remarkably in the patients with edema. It indicated that acupuncture treatment not only had a good antiobesity effect, but also improved the water and salt metabolism of the patients with obesity by the regulation of nervous system and body fluid.
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PMID:[The antiobesity effect of acupuncture and it's influence on water and salt metabolism]. 938 68

A case of hyperaldosteronism caused by adrenal cortical cancer observed in a 32-year-old man was reported. The patient showed marked hypertension and hypokalemia, but neither obesity nor hyperglycemia was observed. Endocrine studies revealed hyperaldosteronism and concurrent excessive secretion of cortisol, but diurnal rhythms of plasma ACTH and cortisol were normal. Imaging studies revealed a large left adrenal mass, and the positive accumulation of radiolabelled material by adrenal scintigraphy was observed both in the tumor and the contralateral adrenal gland. The removed tumor was predominantly composed of dark compact cells with marked nuclear pleomorphism, and mitotic figures and sinusoidal invasion were also observed. The analysis of steroidogenic enzyme activities revealed that the activity of aldosterone-synthesizing enzyme (P-450aldo) which was usually undetectable in normal adrenal tissues and adenomas other than aldosterone-producing adenoma (APA) was detectable as one-third of that of APA. Although activities of other enzymes were reduced, the expression of P-450aldo activity was considered to be the specific character of this cancer.
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PMID:Aldosterone-producing adrenal cortical cancer: a case report and analysis of steroidogenic enzymes in the tumor. 944 88


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