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

The association between arterial hypertension and obesity has been known for many years and demonstrated by epidemiological studies. The physiopathological mechanisms involved consist of increased extracellular volumes, hyperactivity of the sympathetic nervous system and the renin-angiotensin-aldosterone system, and abnormal ion exchanges between extra- and intracellular compartments. Recent studies have demonstrated an association between arterial hypertension and insulin resistance. Insulin resistance may well be the most important aetiological factor in this type of arterial hypertension as it stimulates both renal sodium reabsorption and sympathetic nervous system activity and reduces vascular Na-K-ATPase activity.
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PMID:[Arterial hypertension in patients with obesity. Role of hyperinsulinism and insulin resistance]. 209 34

A possible cause-effect relationship between the decline of mortality from cerebrovascular accidents (CVA) and a better control of arterial hypertension is discussed. The international literature on the subject is critically reviewed in the light of the possible statistical artifacts for enumeration of CVAs, the incidence and fatality of the disease, the prevalence of other risk factors such as hypercholesterolemia, smoking, and the consumption of sodium, potassium and alcohol, and obesity, as well as the contribution of health care.
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PMID:[Treatment of hypertension and the decline of mortality caused by cerebrovascular accidents]. 210 53

Binding equilibria of valproate (2-n-propyl-pentanoic acid anion) with defatted human serum albumin were studied by equilibrium dialysis in a 66 mM sodium phosphate buffer, pH 7.4, 37 degrees. Three hundred and fifty-six observed points for bound versus free valproate concentration were obtained and analyzed in terms of stepwise binding. It was found that the best fit resulted from a model in which 67% of the albumin was capable of binding valproate, whereas 33% did not bind. Thirty acceptable variants of the curve fitting were generated in order to assess the variation of the binding constants. The binding albumin component combines with three molecules of valproate with high affinity and with at least seven additional molecules that are loosely bound. Saturation of the protein cannot be reached. At very high concentrations of free valproate (above 10 mM) irreversible changes in the albumin take place, resulting in poor reproducibility in the amount of bound valproate. In the presence of palmitate, 0.5, 1, and 1.5 mol/mol of albumin, binding of valproate is decreased by a competitive mechanism. It is hypothesized that obesity, developing as a complication of valproate treatment of epilepsy, results from increased availability of long-chain fatty acids due to competitive valproate binding.
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PMID:Valproate and palmitate binding to human serum albumin: an hypothesis on obesity. 211 Oct 5

In the present work I focus on the pathophysiological mechanisms that may explain the association between high sodium intake, obesity and high blood pressure. Despite epidemiological and etiological controversies on the link between excess sodium in the diet and elevated arterial pressure, the association could be explained on the basis of three different pathophysiological mechanisms: (1) abnormal electrolyte transport across cell membranes, a defect that alters sodium/potassium exchange and also sodium/calcium exchanges, increasing the concentration of intracellular calcium ions that heightens vessel wall tension and the smooth muscle process, (2) increased sympathetic nervous system activity and (3) altered cellular sodium concentration that induces waterlogging in the peripheral arteriolar walls. These mechanisms increase peripheral resistance and enhance arterial pressure. Early epidemiological studies documented a strong association between obesity and hypertension; and a greater incidence of high blood pressure and diabetes was reported in persons with upper body obesity (high waist/hip ratio). Researchers have explained obesity-related hypertension accordingly with various mechanisms. Hyperinsulinemia and vascular resistance may trigger the metabolic and adrenergic changes described in obese hypertensive patients in several ways. Insulin may increase absorption of sodium in the diluting segment of the distal nephron with consequent water retention. Alternatively, insulin might alter sodium/potassium distribution thus causing increased vascular peripheral resistance. The increased sodium stimulates adrenergic activity. The water retention in obese subjects increases absolute volume that is predominantly redistributed in the cardiopulmonary area, leading to augmented venous return and cardiac output. These changes in association with a total peripheral resistance considered inappropriately normal, are the main hemodynamic characteristics of obesity-related hypertension.
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PMID:Sodium and obesity in the pathogenesis of hypertension. 215 2

The sensitivity of tissue to insulin is of physiological, pathophysiological and therapeutic relevance. The quantity of insulin and the response to insulin are paramount complementary factors in the regulation of glucose metabolism, and may, at least under certain pathophysiological conditions, also affect cardiovascular function. Hypertension has a high prevalence among subjects with decreased insulin sensitivity and/or hyperinsulinaemia due to obesity, impaired glucose tolerance, non-insulin-dependent diabetes mellitus, and certain other conditions. There is evidence that, even in the absence of obesity or diabetes mellitus, essential hypertension tends to be associated with insulin resistance. The latter elicits a compensatory increase in insulin secretion. Hyperinsulinaemia also occurs in diabetes type 1 as a consequence of insulin treatment. Considering the acute effects of insulin on sympathetic nervous activity, transmembranous cation transport, renal sodium reabsorption, cellular proliferation and lipid metabolism, insulin resistance and/or hyperinsulinaemia may possibly contribute to the genesis of essential, obesity-associated and diabetes-associated hypertension, and may also promote dyslipidaemia in these disorders.
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PMID:Insulin, insulin sensitivity and hypertension. 216 83

Obesity is known to be associated with diabetes, hypertension and hyperlipidemia in the majority of the patients. There could be inaccuracy in measuring the blood pressure in obesity, therefore a cuff of sufficient size is important in blood pressure measurement. All parameters of obesity have been found to have a correlation with hypertension and it has been suggested that change in weight would cause a change in blood pressure. A weight reduction of 12 kg results in a blood pressure fall of 21/13 mm Hg. Such changes in blood pressures have been noted in untreated hypertensives. A few studies have negated the role of change in weight to have any influence on hypertension. Obesity causes a higher cardiac output and higher blood volume leading to hypertension. There may be increased intracellular sodium and reduced sodium-potassium-ATPase activity in obesity which causes increased sodium loading in hypertension. Abnormalities related to the insulin-carbohydrate metabolism and the renin-angiotensin aldosteron system have also been demonstrated in obese patients. Weight reduction also causes reduced dietary salt intake and diminished sympathetic activity. The benefits of weight reduction appear to be directly related to the amount of weight lost.
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PMID:Effect of obesity and weight reduction in hypertension. 218 Feb 41

The aims of this study were to determine whether chronic hyperinsulinemia, comparable to that found in obese hypertensives, elevates mean arterial pressure (MAP) or potentiates the hypertensive effects of angiotensin II (ANG II). Studies were conducted in conscious dogs with kidney mass reduced by 70% in order to increase their susceptibility to hypertensive stimuli. Insulin infusion (0.5 or 1.0 mU.kg-1.min-1 iv) for 7 days with plasma glucose held constant raised plasma insulin more than fivefold but did not increase MAP in four dogs on 138 meq/day Na intake. In seven dogs maintained on a high Na intake (319 meq/day), insulin infusion (1.0 mU.kg-1.min-1) for 28 days raised fasting insulin from 9.8 +/- 1.5 to 56-78 microU/ml but did not increase MAP, which averaged 106 +/- 2 mmHg during control and 102 +/- 2 mmHg during 28 days of insulin infusion. Insulin caused transient sodium and potassium retention followed by renal "escape" that was associated with increased glomerular filtration rate (12-27%). Plasma renin activity and plasma aldosterone were not altered by insulin. In five dogs infused with ANG II (2.0 ng.kg-1.min-1) to cause mild hypertension, insulin infusion (1.0 mU.kg-1.min-1) for 6-28 days did not increase MAP further. Thus chronic hyperinsulinemia did not elevate MAP, even when kidney mass was reduced, and did not potentiate the hypertensive effects of ANG II. These findings suggest that additional factors besides hyperinsulinemia per se are responsible for obesity-associated hypertension.
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PMID:Chronic hyperinsulinemia and blood pressure regulation. 218 Mar 21

Human arterial hypertension is likely a multifactorial trait resulting from multiple measurable monogenes, blended polygenes, shared family environment, and individual environment. Familial aggregation of hypertension and familial correlation of blood pressure appears to be more due to genes than to shared family environment. Total genetic heritability of 80% with some recessive major gene effects have been found for several traits associated with hypertension including urinary kallikrein excretion, intraerythrocytic sodium, and sodium-lithium countertransport. Other interesting factors regarding hypertension genetics include: non-modulation of the renin angiotensin system, intralymphocytic sodium, ionized calcium, and several genetic markers such as haptoglobin, HLA, and MNS blood type. Probably the most clinically useful information regarding the genetics of hypertension is evolving in several studies reporting a strong association of hypertension with dyslipidemia, diabetes, and obesity.
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PMID:Genetics of hypertension: what we know and don't know. 220 56

Hypertension and diabetes mellitus are chronic medical conditions that frequently coexist. In the United States, it is estimated that 10 million persons suffer from diabetes mellitus, 60 million from hypertension, and 3 million from the combination of the two. There may be a causal relationship between hypertension and diabetes. Obesity may be a precipitating factor for both hypertension and non-insulin-dependent diabetes mellitus. Those with insulin-dependent diabetes mellitus generally become hypertensive only with the onset of nephropathy. Glucose tolerance, insulin resistance, and hyperinsulinemia frequently occur with essential hypertension and may be aggravated by hypertension therapy, especially with diuretics and beta-blockers. Hyperinsulinemia may be an important common factor promoting sodium retention, sympathetic nervous system stimulation, and inhibition of the sodium pump. The Working Group on Hypertension in Diabetes has outlined a flexible modified version of the stepped-care approach to the treatment of hypertension in diabetes. Management is complex because diabetes is associated with autonomic neuropathy, sexual dysfunction, hyperlipidemia, and fluid and electrolyte disorders. All these problems can be exacerbated by antihypertensive treatment. Nonpharmacologic measures, which address weight reduction and sodium restriction, are logical, but aggressive antihypertensive medication is invariably necessary. Diuretics and/or beta-blockers were the mainstay of treatment until the introduction of angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers. These newer agents have no deleterious effects on carbohydrate metabolism and are generally better tolerated. Antihypertensive therapy may slow the rate of deterioration in diabetic nephropathy. This was first shown with diuretics, beta-blockers, and hydralazine and more recently with ACE inhibitors, which provide effective blood pressure control and a significant drop in albuminuria without affecting the glomerular filtration rate adversely. ACE inhibition may also lead to increased insulin sensitivity and glucose disposal rate. Long-term trials are needed to assess the effects of these new agents on the treatment of hypertension in the diabetic population.
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PMID:Diabetes mellitus and hypertension. 222 Jul 97

Obese rats maintained on a high-fat diet since weaning were studied to determine whether parasympathetic deficiencies contribute to the cardiovascular malfunction in obesity. Elevations in tail-cuff systolic pressures and plasma insulin indicated that obese rats had borderline hypertension and hyperinsulinemia. Reflex bradycardia produced by angiotensin or phenylephrine in conscious obese rats was less than that in age-matched controls. However, reflex responses elicited by phenylephrine or sodium nitroprusside when the same rats were later anesthetized did not differ between groups. Impairment of afferent or central components of the baroreflex arc was considered unlikely, because depressor, bradycardic, and sympathoinhibitory responses to electrical stimulation of aortic depressor afferents were similar in both rat groups. By contrast, efferent parasympathetic mediation was probably reduced, since depressor and bradycardic responses to electrical stimulation of vagal nerve efferents were significantly smaller in obese than in control rats. Collectively our findings suggest that cardiovascular and baroreflex malfunction in obese rats may result from an autonomic imbalance involving diminished parasympathetic activity.
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PMID:Diminished cardiovascular responsiveness to vagal stimulation in obese rats. 222 Nov 52


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