Cardiovascular Protection (cardiovascular + protection)

Distribution by Scientific Domains


Selected Abstracts


Potential manipulation of endothelial progenitor cells in diabetes and its complications

DIABETES OBESITY & METABOLISM, Issue 7 2010
G. P. Fadini
Diabetes mellitus increases cardiovascular risk through its negative impact on vascular endothelium. Although glucotoxicity and lipotoxicity account for endothelial cell damage, endothelial repair is also affected by diabetes. Endothelial progenitor cells (EPCs) are involved in the maintenance of endothelial homoeostasis and in the process of new vessel formation. For these reasons, EPCs are thought to have a protective impact within the cardiovascular system. In addition, EPCs appear to modulate the functioning of other organs, providing neurotropic signals and promoting repair of the glomerular endothelium. The exact mechanisms by which EPCs provide cardiovascular protection are unknown and the definition of EPCs is not standardized. Notwithstanding these limitations, the literature consistently indicates that EPCs are altered in type 1 and type 2 diabetes and in virtually all diabetic complications. Moreover, experimental models suggest that EPC-based therapies might help prevent or reverse the features of end-organ complications. This identifies EPCs as having a novel pathogenic role in diabetes and being a potential therapeutic target. Several ways of favourably modulating EPCs have been identified, including lifestyle intervention, commonly used medications and cell-based approaches. Herein, we provide a comprehensive overview of EPC pathophysiology and the potential for EPC modulation in diabetes. [source]


Cardiovascular effects of raloxifene: the potential for cardiovascular protection in women

DIABETES OBESITY & METABOLISM, Issue 3 2002
N. K. Wenger
First page of article [source]


Contribution of endothelium-derived hyperpolarizing factors to the regulation of vascular tone in humans

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 4 2008
Jeremy Bellien
Abstract Endothelium plays a crucial role in the regulation of cardiovascular homeostasis through the release of vasoactive factors. Besides nitric oxide (NO) and prostacyclin, increasing evidences show that endothelium-derived hyperpolarizing factors (EDHF) participate in the control of vasomotor tone through the activation of calcium-activated potassium channels. In humans, the role of EDHF has been demonstrated in various vascular beds including coronary, peripheral, skin and venous vessels. The mechanisms of EDHF-type relaxations identified in humans involved the release by the endothelium of hydrogen peroxide, epoxyeicosatrienoic acids (EETs), potassium ions and electronical communication through the gap junctions. The role of EETs could be particularly important because, in addition contributing to the maintenance of the basal tone and endothelium-dependent dilation of conduit arteries, these factors share many vascular protective properties of NO. The alteration of which might be involved in the physiopathology of cardiovascular diseases. The evolution of EDHF availability in human pathology is currently under investigation with some results demonstrating an increase in EDHF release to compensate the loss of NO synthesis and to maintain the endothelial vasomotor function whereas others reported a parallel decrease in NO and EDHF-mediated relaxations. Thus, the modulation of EDHF activity emerges as a new pharmacological target and some existing therapies in particular those affecting the renin,angiotensin system have already been shown to improve endothelial function through hyperpolarizing mechanisms. In this context, the development of new specific pharmacological agents especially those increasing EETs availability may help to prevent endothelial dysfunction and therefore enhance cardiovascular protection in patients. [source]


New Considerations Relating to Class Effect With Angiotensin-Converting Enzyme Inhibitors-The PEACE Study

JOURNAL OF CLINICAL HYPERTENSION, Issue 3 2005
Domenic A. Sica MD
Angiotensin-converting enzyme inhibitor therapy provides positive outcome benefits in a number of cardiac scenarios including congestive heart failure, postmyocardial infarction, as well as in the hypertensive patient at cardiac risk. This benefit exists both in normotensive and hypertensive individuals and is present in those with various grades of cardiovascular risk. This beneficial cardiovascular effect has now been observed with several angiotensin-converting enzyme inhibitors, suggesting a class effect. The Prevention of Events with Angiotensin-Converting Enzyme Inhibition trial studied the effect of adding the angiotensinconverting enzyme inhibitor trandolapril to a contemporary therapeutic regimen of patients with stable coronary artery disease and preserved left ventricular function. In this study, the addition of trandolapril did not confer any additional benefit in terms of reducing the incidence of cardiovascular death, myocardial infarction, or coronary revascularization. The neutral findings in this trial add a new wrinkle to the concept of class effect for cardiovascular protection with angiotensin-converting enzyme inhibitors in patients with coronary artery disease. [source]


Ethanol and red wine polyphenols induce the short-term downregulation of PAI-1 gene expression in vivo in rat aortic endothelium

JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 9 2007
Hernan E Grenett
Abstract Moderate alcohol or red wine consumption reduces the risk of cardiovascular mortality. This cardiovascular protection is likely due to the additive, combined and/or synergistic effects of alcohol itself or other components of wine, in particular polyphenols. Experiments were carried out to determine whether ethanol/polyphenols also decrease plasminogen activator inhibitor type 1 (PAI-1) mRNA expression in vivo, using the rat as an animal model. Male Sprague,Dawley rats were gavaged with ethanol, the individual polyphenols catechin and quercetin or saline vehicle. The in vivo effect of ethanol or individual polyphenols on PAI-1 mRNA was then assessed by in situ hybridisation and quantitative reverse transcriptase (RT) polymerase chain reaction (RT-PCR). PAI-1 mRNA expression was significantly reduced in the endothelial and smooth muscle cells of the thoracic aorta of all experimental rats. RT-PCR analysis of PAI-1 mRNA levels in vascular tissue showed a ,55% reduction in PAI-1 mRNA consistent with the decrease in aortic endothelium PAI-1 mRNA observed with in situ hybridisation. This decrease may enhance endothelial cell (EC)-mediated fibrinolytic activity in vivo. The cardioprotection afforded by moderate red wine consumption can therefore be attributed in part to the combined effects of ethanol and individual polyphenols on EC fibrinolysis. Copyright © 2007 Society of Chemical Industry [source]


Flavonoid inhibition of platelet procoagulant activity and phosphoinositide synthesis

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2003
R. Bucki
Summary., Dietary flavonoids are known for their antiplatelet activity resulting in cardiovascular protection. Phosphatidylinositol 4,5-bisphosphate (PIP2) was previously reported to play a direct role in phosphatidylserine (PS) exposure, as a Ca2+ target. Thrombin formation and platelet procoagulant activity are dependent on PS exposure. As flavonoids can inhibit phosphoinositide (PPI) kinases, we examined whether changes in PPI metabolism in flavonoid-treated platelets could be involved in their antiplatelet effects. Treatment with the flavonoids quercetin or catechin reduced PS exposure, thrombin formation, PIP2 level and resynthesis after platelet activation with collagen, thrombin or calcium ionophore. Flavonoids also prevented [Ca2+]i increase induced by collagen, but not by the ionophore. The ability of flavonoids to decrease PS exposure induced by ionophore treatment could result from the diminution of PIP2 levels, whereas PS exposure induced by collagen could also be diminished by flavonoids' effects on calcium signaling dependent on PIP2 hydrolysis. These data favor a role for PIP2 in the antiplatelet effects of flavonoids. [source]