Abstract
A single exposure to nitric oxide (NO) donors produces a long-lasting hyporesponsiveness to phenylephrine (HRP) in rat aorta rings. Here the authors investigate the role of the endothelial layer in the development of NO-induced HRP and the putative role of endothelium-derived vasoconstrictors in counteracting it. The NO donor S-nitrosoacetyl-D,L-penicillamine (SNAP) induced a dose-dependent reduction in the maximal effect (Emax) of phenylephrine. In rings without endothelium, Emax dropped to 60%, 25%, and 10% of control values 1 h after a 30-min incubation with SNAP (2, 20, and 200 microM, respectively). In contrast, the presence of endothelium prevented the HRP induced by 2 microM SNAP and significantly reduced the HRP elicited by 20 and 200 microM SNAP (Emax reductions of 50% and 65%, respectively), thereby characterizing the endothelium protective effect. Superoxide dismutase (SOD; 100 IU/mL), MnTBAP (a nonenzymatic SOD mimetic; 100 microM), captopril (10 microM), MK886 (a lipoxygenase inhibitor; 10 microM) and BQ 123 (endothelin receptor A antagonist; 1 microM) did not change the endothelium protective effect. Therefore, increased release of vasoconstrictors that would counteract NO-induced loss in phenylephrine responses c...Continue Reading
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Jul 10, 2013·The Journal of Physiology·Olga Yu GashevaDavid C Zawieja
Jun 15, 2007·Nitric Oxide : Biology and Chemistry·Mamadou SarrBernard Muller
Dec 10, 2009·Shock·Thorgerdur SigurdardottirMikael Bodelsson