Endothelin-1 induced proinflammatory markers in the myocardium and leukocytes of guinea-pigs: role of glycoprotein IIB/IIIA receptors.

Aim: To assess whether endothelin-1 (ET-1) induces the in vivo expression of inflammatory-related proteins, namely cyclooxygenase-2 (COX-2) and tissue factor, in the myocardium and circulating leukocytes of guinea-pigs. The involvement of platelets was also analyzed.

Methods: ET-1 (0.

[Effect of HMG-CoA reductase inhibition on endothelial dysfunction-inducing protein in hypercholesterolemic rabbits].

Introduction And Objectives: In our laboratory, we recently obtained evidence that cultured bovine endothelial cells contain cytosolic proteins that form complexes with the 3'-unstranslated region of endothelial nitric oxide synthase (eNOS) mRNA and are associated with its destabilization. The aim of this study was to determine the presence of such proteins and the level of eNOS expression in hypercholesterolemic rabbits as an in vivo model of endothelial dysfunction.

Methods And Results: Endothelium-dependent relaxation in response to acetylcholine was reduced in aortic segments from hypercholesterolemic rabbits compared with controls.

Sevoflurane reduces endothelium-dependent vasorelaxation: role of superoxide anion and endothelin.

Purpose: There are several reports suggesting that volatile anesthetics alter vascular endothelial function. We analyzed the effect of sevoflurane, a fluorinated volatile anesthetic, on nitric oxide (NO)-dependent relaxation, evaluating the role of the endothelium-derived vasoconstrictor endothelin-1 (ET-1).

Methods: The experiments were performed in rat isolated aortic segments aerated in the absence and in the presence of sevoflurane (2%).

Alteration of the soluble guanylate cyclase system in the vascular wall of lead-induced hypertension in rats.

Low-level lead exposure is a known cause of hypertension that has been associated with increased reactive oxygen species activity and endothelial-dependent vasorelaxation impairment. The effect of lead exposure on the vascular nitric oxide (NO)/cyclic guanocine monophosphate (cGMP) system was analyzed. Wistar rats were exposed to 5 ppm lead acetate in the drinking water during 30 d.