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  • 1
    ISSN: 1435-1803
    Keywords: Key words Noradrenaline – nitric oxide – nitric oxide synthase – endothelial cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Altered endothelium-dependent vasodilation has been observed in congestive heart failure (CHF), a disease characterized by a sustained adrenergic activation. The purpose of our study was to test the hypothesis that chronically elevated catecholamines influence the nitric oxide (NO) pathway in the human endothelium. Human umbilical vein endothelial cells (HUVEC) were exposed for 7 days to a concentration of noradrenaline (NA, 1 ng/mL) similar to that found in the blood of patients with CHF. Kinetics of endothelial constitutive NO synthase (ecNOS) and inducible NO synthase (iNOS) activity, measured by [3H]L-arginine to [3H]L-citrulline conversion, and protein expression of ecNOS and iNOS, assessed by Western blot analysis, were unaffected by chronic NA treatment. Furthermore, no changes in subcellular fraction-associated ecNOS were found; this indirectly shows that chronic NA did not cause phosphorylation of the enzyme. Moreover, [3H]L-arginine transport through the plasma membrane was conserved in chronically NA-treated cells. The data demonstrate that prolonged in vitro exposure to pathologic CHF-like NA does not affect the L-arginine NO pathway in human endothelial cells.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-7241
    Keywords: hormones ; renin angiotensin aldosterone ; atrial natriuretic peptide ; tumor necrosis factor alpha ; ACE inhibitors ; heart failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Congestive heart failure is a clinical syndrome in which the capacity of the heart to maintain cardiac output is impaired. As a consequence, blood pressure is threatened and endocrine and paracrine mechanisms are activated to preserve circulatory homeostasis and to maintain blood pressure. At terminal stages, a complex multiorgan syndrome develops with severe pump failure, intense systemic vasoconstriction, and avid water and sodium retention. Increasing evidence points to humoral circulating or locally synthesized substances as one of the causes of the terminal consequences of heart failure. Therefore, the hypothesis that the syndrome of heart failure is, at least in part, a humoral disease has developed and is obtaining scientific credibility. Consequently, the neuroendocrine response to heart failure is no longer viewed as a compensatory beneficial mechanism. Instead, we have learned through the years that pharmacological treatment aimed at reducing the effect of the neuroendocrine response is indeed clinically and prognostically advantageous for the patient.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-7322
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In this review, we have examined the role of oxidative stress and apoptosis in the continuum of molecular changes that accompanies congestive heart failure. Cytokine activation and tumor necrosis factor-α, in particular, may play a role in this continuum, favouring both oxidative stress and apoptosis. Carvedilol, a non selective β- and α-blocker, exerts an anti-apoptotic effect on both the myocytes and the endothelial cells as a consequence of its antioxidant activity. The ability of carvedilol to inhibit apoptosis may have important clinical relevance in congestive heart failure. It is also important to emphasise that, in congestive heart failure, apoptosis occurs, not only in the heart, but also in the periphery. An increased rate of endothelial apoptosis may explain the occurrence of endothelial dysfunction in congestive heart failure.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-7241
    Keywords: angiotensin-converting enzyme ; coronary artery disease ; enalapril ; captopril ; quinapril ; cardiac protection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Clinical and experiments study with angiotensin-converting enzyme (ACE) inhibitors suggest that these agents may improve coronary artery disease by acting at multiple sites in the series of events leading to end-stage heart disease. These agents reduce blood pressure, improve prognosis and symptoms in patients with severe heart failure and in patients after acute myocardial infarction with left ventricular dysfunction. They are useful in the early, acute phase of myocardial infarction. More recently, ACE inhibitors have been shown to reduce in vitro vascular hypertrophy, to attenuate arteriosclerosis, and to maintain endothelium function. Whether these effects occur at clinical levels is still uncertain. The exciting clinical data have led to the proposal that alteration of ACE activity, particularly in tissue, is an important factor in development and progression of CAD. The ACE system is complex, with endocrine, paracrine, and autocrine effects. ACE is present in cardiac and vascular tissue. Therefore, the beneficial effects of ACE inhibitors can be classified as “cardio” and “vasculo” protective. This article summarizes a number of independent and complementary mechanisms pointing to a role of ACE and ACE inhibition in coronary artery disease.
    Type of Medium: Electronic Resource
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