Major differences in gene expression in human coronary smooth muscle cells after nebivolol or metoprolol treatment.

Objective: Vascular smooth muscle cells play a pivotal role in all stages of atherogenesis. Targeting their inflammatory and proliferative qualities might therefore inhibit the progression of atherosclerosis. This study aimed to characterize and compare the effects of the beta-receptor antagonists nebivolol and metoprolol on gene expression in human coronary artery smooth muscle cells (hcaSMC).

Influence of nebivolol and metoprolol on inflammatory mediators in human coronary endothelial or smooth muscle cells. Effects on neointima formation after balloon denudation in carotid arteries of rats treated with nebivolol.

Objective And Background: Inflammation plays a critical role in all stages of atherogenesis. Proliferating vascular smooth muscle cells (SMC) and endothelial cells (EC) enhancing the inflammatory response, both contribute to the progression of atherosclerosis. Anti-proliferative, anti-inflammatory and anti-oxidative therapy seems to be a promising therapeutic strategy.

Secondary syphilis after liver transplantation: case report and review of the literature.

Syphilitic disease is uncommon, but its incidence has increased worldwide in the last few years. An unusual manifestation of secondary syphilis after orthotopic liver transplantation is described which confirms that lues should be considered in patients with immune deficiency and abnormal liver function tests.

Stimulation of serum- and glucocorticoid-regulated kinase-1 gene expression by endothelin-1.

The serum- and glucocorticoid-regulated kinase-1 (SGK1) participates in the regulation of sodium homeostasis and blood pressure by mineralocorticoids. Aldosterone rapidly induces SGK1 transcription, which contributes to the activation of renal epithelial sodium channels. Another important regulator of blood pressure is the vasoactive hormone endothelin-1 (ET-1) that is systemically upregulated in chronic renal failure.

Effects of combined endothelin and angiotensin II antagonism on growth factor-induced proliferation of vascular smooth muscle cells isolated from uremic rats.

Background: The activation of both the renin-angiotensin-aldosterone and endothelin (ET) system in uremia contributes to the development of cardiovascular disease. The combination of ET receptor antagonists and inhibitors of the angiotensin-converting enzyme (ACE) or angiotensin II type 1 (AT,) receptor could therefore inhibit atherogenesis. We studied the effects of different medications on growth-factor-induced proliferation of vascular smooth muscle cells (VSMC) isolated from uremic rats.

Endothelin-1 increases serum-glucocorticoid-regulated kinase-1 expression in smooth muscle cells.

The mechanism of salt-sensitive hypertension is not fully understood. Several studies point to a possible role of endothelin (ET)-1 in this form of hypertension. Serum-regulated and glucocorticoid-regulated kinase-1 (SGK1) mediates trafficking of the renal epithelial sodium channel.

Endothelin-1 regulates protein kinase C isoforms differently in smooth muscle cells and in cardiomyocytes.

Endothelin-1 (ET-1) is known to increase the mitotic response of different growth factors but also to different vasoactive hormones already at threshold concentrations. The aim of this study was to investigate the influence of chronic elevated ET-1 concentrations on protein kinase C (PKC) isoforms in vitro and in vivo. Smooth muscle cells were incubated with ET-1 at a concentration of 10 mol/L.

Influence of growth factors on the proliferation of vascular smooth muscle cells isolated from subtotally nephrectomized rats after endothelin or angiotensin II antagonism.

Background: Cardiovascular disease is the most important cause of death in patients with end-stage renal disease. In uraemia, the renin-angiotensin-aldosterone and endothelin (ET) systems are activated. It is not known whether inhibition of these systems attenuates the proliferation of isolated smooth muscle cells of uraemic rats.

Infectious risk factors for atherosclerotic vascular disease in hemodialysis patients--Chlamydia pneumoniae but not Helicobacter pylori or cytomegalovirus is associated with increased C-reactive protein.

Background: Cardiovascular disease is a major problem in patients with chronic renal failure leading to increased mortality. Several infectious agents have been implicated to be associated with atherosclerosis. We were interested to evaluate whether there is a correlation between a past infection with Chlamydia pneumoniae (Cpn), Helicobacter pylori (Hp) or cytomegalovirus (CMV) and the manifestation of a symptomatic atherosclerotic disease in patients with endstage renal failure.

[Influence of the beta-blocker nebivolol on left ventricular function in patients with chronic heart failure].

Background: Sympathetic activity is a significant predictor of a poor prognosis in heart failure. beta-blockers such as carvedilol, metoprolol or bisoprolol have been shown to improve the prognosis of patients with heart failure.

Aim: This pilot study examined the tolerability and effect of the new beta-blocker nebivolol on left ventricular ejection fraction in patients with chronic heart failure.

Effect of nebivolol on left ventricular function in patients with chronic heart failure: a pilot study.

Background: Sympathetic activity is a significant predictor of a poor prognosis in heart failure. Beta-blockers have been shown to improve the prognosis of patients with heart failure.

Aim: This pilot study examined the tolerability and efficacy of the new beta-blocker nebivolol on left ventricular function in patients with chronic heart failure.

Influence of endothelin receptor antagonists on myocardial protein kinase C isoforms in uraemic cardiomyopathy.

Increased endothelin-1 (ET-1) levels were found in patients with chronic renal failure and these correlate with the severity of renal failure. Increased mortality due to cardiovascular problems is observed in patients with elevated ET-1 concentrations. The aim of this study was to find out the influence of ET-1 and ET receptor antagonists on myocardial protein kinase C (PKC) regulation in uraemic cardiomyopathy.

Chronic elevated endothelin-1 concentrations regulate mitogen-activated protein kinases ERK 1 and ERK 2 in vascular smooth muscle cells.

Increased endothelin-1 (ET-1) levels are found in patients with atherosclerosis. ET-1 is known to increase the mitotic response of different growth factors already at threshold concentrations. The aim of this study was to investigate the influence of ET-1 on the mitogen-activated protein (MAP) kinases, extracellular signal-regulated protein kinase (ERK) 1 and ERK 2.

Modulation of the beta-adrenergic receptor system of vascular smooth muscle cells in vitro and in vivo by chronically elevated endothelin-1 levels.

Endothelin-1 (ET-1) levels are chronically elevated in several cardiovascular diseases and correlate with an increased mortality. However, in contrast to acute biological activities such as vasoconstriction, little is known about long-term effects of ET-1. In this study we determined the effects of ET-1 on the beta(2)-adrenergic receptor (AR) system.