1 Urocortin, an endogenous peptide structurally related to corticotropin-releasing factor (CRF), has potent cardiovascular e ects, suggesting that it may be of signi®cance in cardiovascular regulation. The objective of this study was to analyse the e ects of urocortin and its action mechanisms on human blood vessels. 2 To this, 3 mm long segments from human saphenous veins were prepared for isometric tension recording in an organ bath. 3 In the segments at basal resting tone, urocortin did not produce any e ect, but in the segments precontracted with endothelin-1 (1 ± 10 nM), urocortin (1 pM ± 10 nM) produced concentrationdependent relaxation. 4 This relaxation was not modi®ed by the inhibitor of nitric oxide synthase N G -nitro-L-arginine methyl ester (L-NAME, 100 mM), but it was potentiated by the cyclo-oxygenase inhibitor meclofenamate (10 mM) and it was reduced by the inhibitors of high-conductance Ca 2+ -dependent potassium channels tetraethylammonium (TEA, 10 mM) and charybdotoxin (100 nM). 5 These results indicate that human saphenous veins are very sensitive to urocortin, which produces vascular relaxation by a mechanism independent of nitric oxide and dependent of highconductance Ca 2+ -dependent potassium channels, and that it may be opposed by the release of vasoconstrictor prostanoids. Therefore, urocortin may be of signi®cance for regulation of the venous circulation in humans. British Journal of Pharmacology (2002) 136, 90 ± 94
The results demonstrate that the endothelium-dependent relaxation in forearm veins from controls and non-dialysed patients is mediated by release of nitric oxide and EDHF. In contrast, the relaxation in veins from dialysed patients is mediated mainly by EDHF. EDHF-induced relaxation involves activation of large-conductance Ca2+-activated K+ channels.
OPCABG is associated with less postoperative morbimortality and shorter hospital and intensive care unit length of stay. ONCABG resulted as an independent predictor of morbidity and mortality composite end-point. No statistically significant differences were observed in long-term all-cause mortality between groups.
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