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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A high rate of cardiovascular death in renal patients, particularly patients with endstage renal failure, has not been well appreciated in the past. It is obvious that cardiovascular lesions are more severe than can be explained by the classical risk factors of elevated blood pressure and dyslipidemia. In renal failure, a number of pathomechanisms are operative which may be paradigms of more general relevance, e.g. activation of the renin and sympathetic system, inhibition of the vasoconstrictor NO system, left ventricular hypertrophy in excess of what is expected for high blood pressure. A paradox inverse relation between lipid concentrations and cardiovascular death, i.e. a protective effect of hyperlipidemia, in dialysed patients, presumably results from the confounding effect of malnutrition, high lipid levels being a substitute marker of adequate nutrition.
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PMID:Excess cardiovascular mortality in the uremic patient--what does it teach for other risk factors in the non-renal patient? 773 91

To investigate the pathogenesis of hypertension in patients with obesity and insulin resistance and to explore the role of plasma lipids, we studied 30 subjects at the end of 7 days of low (20 mEq/d) then high (200 mEq/d) sodium diets. Glucose and insulin tolerance tests were performed at the end of each week and blood and urine collected for measurements of plasma aldosterone, renin activity, electrolytes, insulin, and lipoproteins. There was a strong negative correlation between plasma aldosterone and high-density lipoprotein cholesterol during both diets. There were weaker positive correlations between plasma aldosterone and insulin or triglycerides. When the aldosterone-renin ratio was the dependent variable and the correlation controlled for serum potassium, the inverse relationship with high-density lipoprotein cholesterol and the positive correlation with insulin remained, but only during the high salt diet. Subjects were divided into three groups based on high-density lipoprotein cholesterol. Subjects with the lowest high-density lipoprotein cholesterol levels showed the highest aldosterone, plasma triglycerides, body mass index, and waist-to-hip ratio. Those subjects also demonstrated the greatest resistance to insulin action on glucose and plasma unesterified fatty acids. There was a weak direct correlation between plasma aldosterone and systolic blood pressure during the high salt diet. These data suggest that high aldosterone levels may be a link between dyslipidemia, insulin resistance, and hypertension, a relationship made more evident by high salt intake.
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PMID:Relationships among plasma aldosterone, high-density lipoprotein cholesterol, and insulin in humans. 784 50

A positive association exists between insulin resistance, dyslipidemia, and hypertension, specifically salt-sensitive hypertension. A subgroup of salt-sensitive normal and high renin hypertensives called nonmodulators (NM) manifest an inability to modulate the adrenal and renal blood flow responses to a change in dietary sodium. Therefore, we tested the hypothesis that the NM subgroup would be insulin resistant and dyslipidemic when compared with normal and high renin hypertensives, in whom modulation is intact (M). Forty-six nondiabetic hypertensive individuals were evaluated and their modulation status defined by either renal or adrenal criteria. Fasting blood was drawn for measurement of several metabolic factors. Since the NM group had a greater body mass index (BMI) it was subdivided into a "lean" subgroup that matched the BMI of the M group. The fasting insulin levels in both the total NM and lean NM groups was significantly higher than in the M group (P = .013 and .04, respectively). There were no differences in age, blood pressure, or plasma/serum levels of glucose, triglycerides, total cholesterol, or potassium. NM had elevated fasting insulin levels compared to M, compatible with an insulin resistant state, but this insulin resistance are dissociable in the hypertensive population.
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PMID:Metabolic derangements in nonmodulating hypertension. 854 Oct 1

During the last decade, our understanding of the role of nitric oxide for central renal functions has greatly been enhanced. We know now that nitric oxide is produced in renal arteries, macula densa, glomeruli, and tubules by different NO-synthases. Nitric oxide contributes to physiological regulation of renal blood flow, renal autoregulation, tubuloglomerular feedback, renin release, pressure natriuresis, and tubular function. The physiological role of nitric oxide can be modulated by a variety of pathophysiological influences, such as dyslipidemia, diabetes mellitus, hypertension, specific drugs, or radiocontrast agents. In this article, the possible interactions between nitric oxide and atherogenic lipoproteins with regard to important renal functions and development of glomerulosclerosis have been stressed. Atherogenic lipoproteins impair endothelium-dependent, nitric oxide-mediated dilations of renal arteries. The underlying mechanism involves formation of reactive oxygen species which inactivate nitric oxide. Lipoproteins induce formation of oxygen radicals not only in arteries, but also in glomeruli and juxtaglomerular cells, causing, e.g., stimulation of renin release. Although interactions between lipoprotein and nitric oxide take place at different levels, they finally may contribute to renovascular hypertension. Future studies will have to prove that treating hyperlipidemia has a positive influence on nitric oxide-mediated renal functions.
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PMID:Impact of nitric oxide on renal hemodynamics and glomerular function: modulation by atherogenic lipoproteins? 881 12

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

To investigate whether molecular variation in the renin gene contributes to the greater blood pressure of spontaneously hypertensive rats (SHR) versus normotensive Brown Norway (BN) rats, we measured blood pressure in an SHR progenitor strain and an SHR congenic strain that are genetically identical except at the renin gene and an associated segment of chromosome 13 transferred from the BN strain. Backcross breeding and molecular selection at the renin locus were used to create the SHR congenic strain (designated SHR.BN-Ren) that carries the renin gene transferred from the normotensive BN strain. We found that transfer of the renin gene from the BN strain onto the genetic background of the SHR did not decrease blood pressure in rats fed either a normal or high-salt diet. In fact, the systolic blood pressures of the SHR congenic rats tended to be slightly greater than the systolic blood pressures of the SHR progenitor rats. However, the congenic strain exhibited lower serum high-density lipoprotein cholesterol, and greater levels of total cholesterol, very-low-density lipoprotein, and intermediate-density lipoprotein cholesterol during administration of a high-fat, high-cholesterol diet. These findings demonstrate that (1) under the environmental circumstances of the current study, the greater blood pressure of SHR versus BN rats cannot be explained by strain differences in the renin gene and (2) a quantitative trait locus affecting lipid metabolism exists on chromosome 13 within the transferred chromosome segment. The SHR.BN-Ren congenic strain may provide a useful new animal model for studying the interaction between high blood pressure and dyslipidemia in cardiovascular disease.
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PMID:Effect of renin gene transfer on blood pressure in the spontaneously hypertensive rat. 945 31

The recent decrease of cardiovascular mortality in the USA is less pronounced than it has been in the preceding three decades. Elsewhere, cardiovascular mortality decreased and in some countries it increased. Cerebrovascular disease and ischemic heart disease were responsible for 21% of deaths recorded by the World Health Organization in 1990 and 1997, of which hypertension was estimated to be directly responsible for half of these deaths. Apart from blood pressure (BP) elevation, essential hypertension is frequently associated with factors that increase the risk of poor cardiovascular outcomes: insulin resistance/dyslipidemia, elevated angiotensin and norepinephrine, a tendency for hypercoagulability, platelet overactivity, tachycardia, vulnerability to arrhythmias, vascular hypertrophy, endothelial dysfunction, and left ventricular hypertrophy. Excess activation of the renin-angiotensin system, independent of BP elevation, contributes to these abnormalities. To achieve better results in the future, focus must be shifted from BP lowering to recognition of specific effects of drugs on these diverse pathophysiologic aspects of hypertension. The Valsartan Antihypertensive Long-term Use Evaluation (VALUE) trial, which is evaluating the effect of valsartan (Diovan((R))) vs. amlodipine, is a milestone in the effort to test whether newer compounds offer a better reduction of the cardiovascular consequences of hypertension, as well as good BP control. The hypothesis is that valsartan by antagonizing the negative effects of angiotensin on smooth muscle cell growth, endothelial function, sympathetic overactivity, and coagulation, may have for the same degree of BP lowering, better protective effects than the leading calcium antagonist amlodipine.
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PMID:Long-term potential of angiotensin receptor blockade for cardiovascular protection in hypertension: the VALUE trial. Valsartan Antihypertensive Long-term Use Evaluation. 1044 89

Cardiovascular disease remains a frequent cause of morbidity and mortality in industrialized countries, particularly in subjects with hypertension, diabetes mellitus, and dyslipidemia, conditions frequently associated with central obesity. Identification of early morphological and/or functional alterations of the cardiovascular system may help target individuals most likely to benefit from preventive measures. The literature data and our own experience suggest that parameters that are direct expressions of cardiovascular damage, can be identified at an early stage. For example, diastolic dysfunction may precede the clinical expression of several cardiac diseases, left ventricular hypertrophy is one of the first manifestations of cardiac involvement in hypertension, central obesity and diabetes mellitus, and a carotid plaque may point to concomitant coronary artery disease. Other early manifestations of cardiovascular involvement are microalbuminuria and endothelial dysfunction. Insulin resistance and alterations of the renin-angiotensin-aldosterone system play an important physiopathogenic role in the development of cardiovascular damage in obese subjects, and their association with risk and cardiovascular disease has been confirmed in numerous studies. Since all these changes generally precede overt clinical manifestations and are closely related to cardiovascular morbidity, they may help identify individuals at the highest risk of cardiovascular events.
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PMID:Early markers of cardiovascular damage in obese subjects. 1072 13

The management of diabetic hypertension requires meticulous selection of agents in the antihypertension armamentorium. There may be several associated factors to be considered while treating a hypertensive diabetic. These include hyperglycemia, dyslipidemia, proteinuria, left ventricular hypertrophy and heart failure to name a few. Losartan is the first of a new class of agents in the list of antihypertensive drugs. By its selective angiotension II receptor (subtype AT1) blocking action it is postulated to bring about a more complete inhibition of the renin-angiotensin system. Thus, it might produce all the benefits of angiotensin converting enzyme (ACE) inhibitor therapy with the freedom from cough so commonly seen with the use of ACE inhibitors. This review attempts to analyze the possible benefits of losartan therapy in diabetes.
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PMID:Role of losartan therapy in the management of diabetic hypertension. 1127 47


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