Impact of lipid and ACE inhibitor therapy on cardiovascular disease and metabolic abnormalities in the diabetic and hypertensive patient

Sowers, J. R.

doi:10.1038/sj.jhh.1000394

Cited by 44 publications

(3 citation statements)

References 8 publications

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“…Hypertension is associated with increased insulin resistance, which leads to low serum HDL levels (57,58). ACE-Is and ARBs may raise serum HDL concentration by increasing insulin sensitivity (14,17,59,60).…”

Section: Discussionmentioning

confidence: 99%

Effect of Antihypertensive Treatment on PlasmaFibrinogen and Serum HDL Levelsin Patients with Essential Hypertension

Papadakis

Mikhailidis

Vrentzos

et al. 2005

Clin Appl Thromb Hemost

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The influence of hypertension, and its treatment, on circulating lipid and fibrinogen (Fib) concentrations in patients with essential hypertension was investigated. The lipid profile and Fib levels were measured in 353 patients (131 men) with essential hypertension. Their median age was 60 years (range: 18-85 years). All patients had normal results from liver, renal, and thyroid function tests. There were 162 patients (45.9%) who were not receiving antihypertensive treatment. Of the remaining patients, 117 were taking 'lipid-hostile' beta-blockers, thiazide diuretics) antihypertensives and 74 were taking 'lipid-neutral' (angiotensin-converting enzyme inhibitors, calcium channel blockers, angiotensin-II receptor blockers) agents. Patients who were taking 'lipid-hostile' antihypertensive drugs had significantly higher plasma Fib concentrations when compared with those taking 'lipid-neutral' antihypertensives or those not receiving antihypertensive treatment. These differences were not attributable to established factors that influence plasma Fib levels, since when smokers and patients with diabetes mellitus and/or vascular disease were excluded, the difference remained significant. In addition, in these more homogeneous groups, patients receiving 'lipid-neutral' treatment had significantly higher serum high-density lipoprotein (HDL) cholesterol levels when compared with both those taking 'lipid-hostile' antihypertensives and untreated ones. There were no significant differences in the other lipid variables, independently of the presence/absence or the type of antihypertensives. These results suggest that antihypertensive drugs have additional effects, beyond lowering blood pressure, on other vascular risk factors, like Fib and HDL. These effects may depend on the type of drug used.

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Section: Discussionmentioning

confidence: 99%

Effect of Antihypertensive Treatment on PlasmaFibrinogen and Serum HDL Levelsin Patients with Essential Hypertension

Papadakis

Mikhailidis

Vrentzos

et al. 2005

Clin Appl Thromb Hemost

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“…Several mechanisms affecting TG levels also have an effect on HDL levels, and viceversa (Arnon et al 1993;Brinton et al 1994;Deeb et al 2003;Kwiterovich 2000). Combined low HDL and elevated TG have been reported to be frequently observed in essential hypertension (Sowers 1997), myocardial infarction (Ballantyne et al 2001), and stroke (Lindenstrom et al 1994), as well as in several inherited disorders of lipid and lipoprotein metabolism, including familial combined hyperlipidemia (FCHL) (Brunzell et al 1983;Edwards et al 1999). However, the implication of TG as an independent CVD risk factor has been debated for many years, with several authors suggesting that the TG effect is secondary to its relationship to other lipid-related traits, and most particularly to HDL (Fruchart and Duriez 2002;Havel 1988).…”

Section: Introductionmentioning

confidence: 94%

Genome scan for quantitative trait loci influencing HDL levels: evidence for multilocus inheritance in familial combined hyperlipidemia

et al. 2005

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Several genome scans in search of high-density lipoprotein (HDL) quantitative trait loci (QTLs) have been performed. However, to date the actual identification of genes implicated in the regulation of common forms of HDL abnormalities remains unsuccessful. This may be due, in part, to the oligogenic and multivariate nature of HDL regulation, and potentially, pleiotropy affecting HDL and other lipid-related traits. Using a Bayesian Markov Chain Monte Carlo (MCMC) approach, we recently provided evidence of linkage of HDL level variation to the APOA1-C3-A4-A5 gene complex, in familial combined hyperlipidemia pedigrees, with an estimated number of two to three large QTLs remaining to be identified. We also presented results consistent with pleiotropy affecting HDL and triglycerides at the APOA1-C3-A4-A5 gene complex. Here we use the same MCMC analytic strategy, which allows for oligogenic trait models, as well as simultaneous incorporation of covariates, in the context of multipoint analysis. We now present results from a genome scan in search for the additional HDL QTLs in these pedigrees. We provide evidence of linkage for additional HDL QTLs on chromosomes 3p14 and 13q32, with results on chromosome 3 further supported by maximum parametric and variance component LOD scores of 3.0 and 2.6, respectively. Weaker evidence of linkage was also obtained for 7q32, 12q12, 14q31-32 and 16q23-24.

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“…Decreased high-density lipoproteins (HDL) together with increased plasma levels of low-density (LDL) and very low-density lipoproteins (VLDL), as well as hypertriglyceridemia, hypercholesterolemia, and insulin resistance, were found in many hypertensive patients. 3,4 There is increasing evidence for a genetic basis for the association of hypertension with insulin resistance and dyslipidemia. The genetic locus associated with dyslipidemia accompanying hypertension or diabetes seems to be closely linked to the LDL receptor and insulin receptor locus.…”

mentioning

confidence: 99%

Abnormalities of membrane function and lipid metabolism in hypertension A review

Zicha

Kuneš

Devynck

1999

American Journal of Hypertension

208

175

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Hypertension, which is characterized by multiple alterations in the structure and function of the cell membrane, is often associated with important metabolic abnormalities including those concerning lipid metabolism. Dyslipidemia accompanying essential hypertension consists of elevated plasma triglycerides, low HDL cholesterol, and increased levels of atherogenic LDL cholesterol particles. The altered membrane microviscosity seen in hypertensive subjects reflects the changes of membrane lipid composition resulting from intensive exchange between circulating and membrane lipids, as well as from abnormal cellular lipid synthesis and metabolism. The changes of membrane microviscosity are known to modulate the activity of proteins involved in ion transport, signal transduction, cell Ca 2؉ handling, intracellular pH regulation, etc. Alterations in plasma or membrane lipids are indeed closely associated with ion transport abnormalities as well as with impaired control of cytosolic Ca 2؉ T here is no doubt that essential hypertension is associated with multiple membrane alterations, including changes in membrane microviscosity, receptor function, signal transduction, ion transport, calcium mobilization, intracellular pH regulation, and so on. Lipids, as an integral part of the cell membrane, play a decisive role in the modulation of the membrane properties mentioned. Specific lipid-lipid and lipid-protein interactions result in a highly dynamic but precisely controlled architecture of membrane components. Major regulators of membrane architecture are membrane potential, intracellular Ca 2ϩ and pH, lipid composition, cell-to-cell contact, and membrane coupling with the cytoskeleton or extracellular matrix. Intermolecular associations in the membrane and at the membrane-cytoskeleton interface are further selectively controlled by specific phosphorylation and dephosphorylation cascades involving both proteins and lipids. This is regulated by the extracellular matrix as well as by the binding of growth factors and hormones to their specific receptors. 1,2The aim of this review is to outline some interrelationships between abnormal lipid metabolism and altered membrane structure or function in human and experimental hypertension, and to evaluate whether abnormal lipid metabolism, which is responsible for a great part of membrane abnormalities found in hypertension, might be an integral part of its pathogenetic mechanisms. BLOOD PRESSUREMultiple metabolic abnormalities often accompany essential hypertension. Decreased high-density lipoproteins (HDL) together with increased plasma levels of low-density (LDL) and very low-density lipoproteins (VLDL), as well as hypertriglyceridemia, hypercholesterolemia, and insulin resistance, were found in many hypertensive patients. 3,4 There is increasing evidence for a genetic basis for the association of hypertension with insulin resistance and dyslipidemia. The genetic locus associated with dyslipidemia accompanying hypertension or diabetes seems to be closely linked to the LDL recept...

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Impact of lipid and ACE inhibitor therapy on cardiovascular disease and metabolic abnormalities in the diabetic and hypertensive patient

Cited by 44 publications

References 8 publications

Effect of Antihypertensive Treatment on PlasmaFibrinogen and Serum HDL Levelsin Patients with Essential Hypertension

Effect of Antihypertensive Treatment on PlasmaFibrinogen and Serum HDL Levelsin Patients with Essential Hypertension

Genome scan for quantitative trait loci influencing HDL levels: evidence for multilocus inheritance in familial combined hyperlipidemia

Abnormalities of membrane function and lipid metabolism in hypertension A review

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