Meanings of endothelial nitric in English

Loss of endothelial nitric oxide bioavailability is implicated in pulmonary hypertension pathogenesis.

These effects were accompanied by activation of myocardial Akt and endothelial nitric oxide synthase.

Western blots revealed similar endothelial nitric oxide (NO) synthase expression in all three vessels.

No endothelial nitric oxide synthase type III expression was found in the media of great saphenous veins.

The effects may be partly due to its capacity to stimulate endothelial nitric oxide synthase (eNOS).

The role of endothelial nitric oxide synthase (eNOS) in endothelial dysfunction induced by sepsis is controversial.

A number of studies have demonstrated that dihydropyridine calcium antagonists enhance bioavailability of endothelial nitric oxide (NO).

This was associated with higher levels of active (phosphorylated serine 1177) endothelial nitric oxide synthase in their kidneys.

In late sepsis, both nitric oxide-dependent relaxation responses and endothelial nitric oxide synthase levels were decreased in septic mice arteries.

This was accompanied by increment of hepatocytes proliferation, and expression of vascular endothelial growth factor and endothelial nitric oxide synthase.

The latter hampered the detachment of endothelial nitric oxide synthase from caveolin-1, leading to an impairment of nitric oxide signaling.

Western blot analyses revealed upregulation of Akt- endothelial nitric oxide-nitric oxide-cGMP-GS3Kβ signaling early in the progression of hypertrophy and heart failure.

However, the internal thoracic artery shows a higher intensity of endothelial nitric oxide synthase type III expression, particularly within the media.

These effects of BH4 were mediated through the regulation of nitric oxide compared with superoxide synthesis by endothelial nitric oxide synthase.

Cytoprotective SBwE substantially reduced the sustained high glucose-induced expression of endothelial nitric oxide synthase and attenuated the formation of peroxynitrite radicals.

MG-132 could reverse the decrease in endothelial nitric oxide synthase expression and improve nitric oxide-dependent vasodilator dysfunction in septic mice arteries.