Muscle metaboreflex is blunted with reduced vascular resistance response of nonexercised limb in patients with chronic heart failure.

Background: Exercise-mediated muscle metaboreflex (MMR) activates the sympathetic nervous system afferently and may play an important role in the reduction in blood flow in nonexercised limb, thus enhancing exercised skeletal muscle blood flow (ie, normal regional blood flow redistribution during exercise). However, few data are available to describe the relationship between MMR and peripheral vascular control during exercise in congestive heart failure (CHF). The aim of this study was to determine whether MMR is impaired in CHF, and, if so, whether MMR is related to clinical severity of CHF and to changes in nonexercised limb vascular resistance in CHF.

Endothelial dysfunction in patients with peripheral arterial disease and chronic hyperhomocysteinemia: potential role of ADMA.

Hyperhomocysteinemia is associated with an enhanced risk for cardiovascular disease. Patients with peripheral arterial disease (PAD) show an increased prevalence of hyperhomocysteinemia. A decreased biological activity of nitric oxide (NO) may contribute to homocysteine-associated endothelial dysfunction.

Reduced vascular compliance is associated with impaired endothelium-dependent dilatation in the brachial artery of patients with congestive heart failure.

Background: Alterations in elastic properties and vascular structure of conduit vessels are important detrimental factors contributing to increased cardiac load and reduced tissue perfusion in patients with congestive heart failure (CHF). It has been demonstrated that endothelial function in the peripheral vasculature is impaired in this disorder, which may induce abnormal vascular elastic properties and remodeling. However, it remains unknown whether changes in vascular structure or mechanical properties are related to endothelial dysfunction in conduit arteries of patients with CHF.

ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of L-arginine and B vitamins.

Objectives: Hyperhomocyst(e)inemia is a risk factor for atherosclerotic vascular disease, and it is associated with endothelial dysfunction. Mechanisms responsible for endothelial dysfunction in hyperhomocyst(e)inemia may involve impaired bioavailability of NO, possibly secondary to accumulation of the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) and increased oxidative stress. We investigated whether oral treatment with B vitamins or L-arginine normalizes endothelium-dependent, flow-dependent vasodilation (FDD) in patients with peripheral arterial occlusive disease (PAOD) and hyperhomocyst(e)inemia.

Effects of chronic subdepressor dose of angiotensin II type 1 receptor antagonist on endothelium-dependent vasodilation in patients with congestive heart failure.

Angiotensin II type 1 receptor antagonist (AIIRA) has been reported to improve exercise capacity and prognosis in patients with congestive heart failure (CHF). However, the effects of AIIRA on peripheral endothelium-dependent and -independent vasodilation remain undefined in this disorder. This study examined the effects and the mechanism of chronic AIIRA therapy on peripheral vasomotion in CHF.

Nitric oxide plays an insignificant role in direct vasodilator effects of calcium channel blockers in healthy humans.

Several experimental studies have suggested that the vasodilatory effects of calcium channel blockers (CCBs) are due in part to an endothelium-dependent mechanism. However, it remains unknown whether CCBs directly augment liberation of endothelium-derived dilator substances such as nitric oxide (NO) in the human vasculature. The aim of this study was to examine whether CCBs of several kinds directly increase the bioavailability of NO in forearm resistance vessels.