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pubmed-article:15115984pubmed:abstractTextInhaled nitric oxide produces potent pulmonary vasodilation by activating soluble guanylate cyclase and increasing smooth muscle cell concentrations of cyclic guanosine monophosphate. However, responses are often nonsustained, and clinically significant increases in pulmonary vascular resistance have been noted on its acute withdrawal. In vitro and in vivo data suggest that inhaled nitric oxide decreases endogenous nitric oxide synthase activity. The effects of inhaled nitric oxide on the downstream mediators of the nitric oxide/cyclic guanosine monophosphate cascade, soluble guanylate cyclase and phosphodiesterase 5, have not been investigated. We sought to determine the effects of inhaled nitric oxide on endogenous cyclic guanosine monophosphate levels, soluble guanylate cyclase, and phosphodiesterase 5 protein levels in the intact lamb.lld:pubmed
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pubmed-article:15115984pubmed:articleTitleInhaled nitric oxide decreases pulmonary soluble guanylate cyclase protein levels in 1-month-old lambs.lld:pubmed
pubmed-article:15115984pubmed:affiliationDepartment of Cardiothoracic Surgery, University of California, San Francisco 94143-0106, USA.lld:pubmed
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