Effects of low habitual cocoa intake on blood pressure and bioactive nitric oxide: a randomized controlled trial.

Context: Regular intake of cocoa-containing foods is linked to lower cardiovascular mortality in observational studies. Short-term interventions of at most 2 weeks indicate that high doses of cocoa can improve endothelial function and reduce blood pressure (BP) due to the action of the cocoa polyphenols, but the clinical effect of low habitual cocoa intake on BP and the underlying BP-lowering mechanisms are unclear.

Objective: To determine effects of low doses of polyphenol-rich dark chocolate on BP.

Effect of cocoa and tea intake on blood pressure: a meta-analysis.

Background: Epidemiological evidence suggests blood pressure-lowering effects of cocoa and tea. We undertook a meta-analysis of randomized controlled trials to determine changes in systolic and diastolic blood pressure due to the intake of cocoa products or black and green tea.

Methods: MEDLINE, EMBASE, SCOPUS, Science Citation Index, and the Cochrane Controlled Trials Register were searched from 1966 until October 2006 for studies in parallel group or crossover design involving 10 or more adults in whom blood pressure was assessed before and after receiving cocoa products or black or green tea for at least 7 days.

Endothelial antioxidant actions of dihydropyridines and angiotensin converting enzyme inhibitors.

Dihydropyridines and angiotensin converting enzyme inhibitor effects on superoxide and nitric oxide (NO) were compared in high glucose (20 mM, 24 h)-treated human Ea.hy 926 endothelial cells. High glucose stimulated superoxide both extracellularly (lucigenin chemiluminescence, cytochrome c reduction) and intracellularly (dihydrorhodamine 123 fluorescence).

Antioxidant and nitric oxide-sparing actions of dihydropyridines and ACE inhibitors differ in human endothelial cells.

The effects of dihydropyridine Ca2+ channel blockers (DHP) and ACE inhibitors on superoxide formation and nitric oxide (NO) bioavailability were compared in human EA.Hy926 endothelial cells (EC). EC were stimulated 4 h with angiotensin II (Ang II, 10 nM) +/- study drugs.

Different antioxidative potencies of dihydropyridine calcium channel modulators in various models.

There is evidence that dihydropyridine calcium antagonists (DHP) play a beneficial role during the development of atherosclerosis. Since antioxidative properties of this substance class may be important, we investigated the antioxidative potency of the DHP prototype calcium channel antagonist nifedipine, the long acting calcium channel antagonist lacidipine, the DHP calcium channel agonist Bay K 8644 and the bulky DHP derivate Bay O 5572 (negligible effects on L-type calcium channels) in three different models. Additionally, we examined the potential correlation between lipophilic and antioxidative properties.

Acute effects of glucose and insulin on vascular endothelium.

Aims/hypothesis: Chronic exposure to high concentrations of glucose has consistently been demonstrated to impair endothelium-dependent, nitric oxide (NO)-mediated vasodilation. In contrast, several clinical investigations have reported that acute exposure to high glucose, alone or in combination with insulin, triggers vasodilation. The aim of this study was to examine whether elevated glucose itself stimulates endothelial NO formation or enhances insulin-mediated endothelial NO release.

Measurement of nitric oxide by reconversion of nitrate/nitrite to NO.

A simple and sensitive method is presented to measure the unstable molecule nitric oxide (NO) by reconversion of nitrate/nitrite to NO. Nitrate and nitrite are the stable degradation products of NO that accumulate in supernatants of biological samples that release nitric oxide. First, nitrate is enzymatically converted to nitrite using nitrate reductase.

Reaction rate constants of superoxide scavenging by plant antioxidants.

Plant phenols may exert protective effects by scavenging superoxide, which is implicated in tissue damage and accelerated inactivation of vasorelaxing nitric oxide. Preventing the interaction of superoxide with tissue biomolecules depends not only on the extent of superoxide scavenging but also on scavenging velocity. However, information on superoxide scavenging kinetics of plant phenols is scarce.

Amlodipine increases endothelial nitric oxide by dual mechanisms.

Several experimental and clinical studies have demonstrated the antiatherogenic profile of the long-acting calcium antagonist amlodipine. Given the pivotal role of endothelial (dys)function during atherogenesis, we investigated the influence of amlodipine on endothelial nitric oxide (NO) bioavailability. Acute addition of amlodipine to segments of porcine coronary arteries resulted in a significant increase in NO release which could be blocked by the NO synthase inhibitor L-NMMA (N-monomethylarginine).

The HMG-CoA reductase inhibitor cerivastatin enhances the nitric oxide bioavailability of the endothelium.

The aim of this study was to investigate whether the HMG-CoA reductase inhibitor cerivastatin alters the nitric oxide (NO) bioavailability of porcine aortic endothelial cell cultures and of native porcine coronary endothelium, after short-term (minutes) and long-term (24-hour) treatment with cerivastatin (electrochemical NO sensor). NO-synthase expression (Western blot, ELISA) and activity (3H-arginine assay) after cerivastatin treatment were determined. Furthermore, the authors investigated whether cerivastatin modulates an angiotensin II (10 micromol/L; 4 hours) induced reactive oxygen species (ROS) release from intact vessels (lucigenin-enhanced chemiluminescence-assay).

Nitric oxide formation and corresponding relaxation of porcine coronary arteries induced by plant phenols: essential structural features.

The high intake of polyphenols is thought to contribute to the beneficial cardiovascular effects of plant-centered diets. A putative mechanism underlying the cardioprotective activity is thought to be a plant phenol-induced increase of nitric oxide formation by the constitutive endothelial nitric oxide synthase. Twenty-eight phenols of different classes commonly occurring in plant foods were examined for their capability of enhancing the endothelial nitric oxide release of isolated porcine coronary arteries by direct real-time measurement of the luminal surface nitric oxide concentration with an amperometric microsensor.

Nisoldipine increases the bioavailability of endothelial NO.

Different observations suggest that dihydropyridine calcium antagonists alter endothelial NO release. Therefore, in a first step we investigated whether part of the nisoldipine (a dihydropyridine calcium antagonist with a possible selectivity for coronaries)-induced vasorelaxation was due to an NO release from the endothelium in porcine coronary arteries. Secondly, we directly measured whether nisoldipine increased NO release from rabbit aorta or the nisoldipine enantiomers (Bay R 1223, Bay R 1224) from rat aorta.

Nifedipine increases endothelial nitric oxide bioavailability by antioxidative mechanisms.

Short-term treatment of the endothelium with dihydropyridine calcium antagonists resulted in an increased release in NO that is not due to a modulation of L-type calcium channels, because macrovascular endothelial cells do not express this channel. We investigated whether long-term (48 hours) treatment of porcine endothelial cell cultures with the dihydropyridine calcium antagonist nifedipine resulted in a similar enhanced NO liberation. Regarding to the underlying mechanism, we examined whether (1) nifedipine changed the mRNA and protein levels of the constitutive endothelial NO synthase (NOS) in endothelial cell cultures or (2) nifedipine exerts an NO protective effect via its antioxidative properties, as revealed in a cell culture model and with native endothelium from porcine coronary arteries.

A new method to measure nitrate/nitrite with a NO-sensitive electrode.

There are different methods to measure the unstable molecule nitric oxide (NO). We will describe a new sensitive method to measure NO by reconversion of nitrate/nitrite to NO, which will be determined with an amperometric Clark-type electrode. Nitrate and nitrite are the degradation products of NO.

Simultaneous measurement of intracellular Ca(2+) and nitric oxide: a new method.

Different methods to measure the unstable radical nitric oxide (NO) have been established. We are going to present a new method to measure intracellular calcium and NO simultaneously in endothelial cells. A new fluorescent dye (DAF-2) has been developed recently which binds NO resulting in an enhanced fluorescence.

Nifedipine and Bay K 8644 Induce an increase of.

BACKGROUND: The dihydropyridine-induced vasorelaxation is partly dependent on the endothelium, which does not express L-type calcium channels. Because nitric oxide (NO) is one of the most important endothelium-derived vasorelaxing factors, we investigated how the calcium antagonist nifedipine and the calcium agonist Bay K 8644 modulate intracellular calcium and NO formation in porcine endothelial cells. METHODS AND RESULTS: NO formation of porcine aortic endothelial cell cultures and of native endothelium of intact porcine coronary arteries was measured with an electrochemical electrode, and the intracellular concentration of Ca(2+) [Ca(2+)](i) was evaluated using the Fura-2 technique.

Nitric oxide causes a cGMP-independent intracellular calcium rise in porcine endothelial cells-a paradox?

This study was undertaken to investigate the influence of exogenous NO on intracellular calcium levels of porcine aortic endothelial cell culture monolayers. Spontaneous NO liberating substances with different half-life periods (NOC-9 [10 micromol/L] approximately 1 min, SNAP [10 micromol/L] approximately 4 h), and an aqueous NO gas solution [130 nmol/L] were added onto the monolayers. All three solutions induced a rapid and similar calcium rise in the endothelial cells.

Epicardial image analysis using a desk top computer. Comparison of epicardial flow distribution and NADH-fluorescence pattern.

In isolated coronary-ligated rabbit hearts, quantification of epicardial flow distribution pattern and of ischemic area was performed from flow indicator and endogenous NADH-fluorescence pictures, respectively, after UV-flash photography. After being digitized (256 X 256 pixels), the fluorescence photos were analyzed by an Apple desk computer using self-written software (fast machine routines called from BASIC programs). The ischemic area (= sum of pixels with enhanced NADH fluorescence) corresponds to the area with disturbed coronary perfusion (= sum of pixels with diminished indicator fluorescence).