Inhibition of nitric oxide synthase by chronic L-NAME administration increases circulating endothelin levels in an in vivo guinea pig model, supporting an inverse regulatory relationship between nitric oxide and endothelin.
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Endothelin and nitric oxide are both endothelium-derived vasoactive factors which appear to play a role in a variety of circulatory disorders (Leppaluoto and Ruskoaho, 1992; Moncada et al., 1991; Nathan, 1992; Rubanyi and Parker Botelho, 1991). Boulanger and Lüscher (1990) noted in isolated blood vessels that the release of endothelin and nitric oxide were inversely related. The intracellular levels of cGMP appear to be the determinant of this response, i.e., nitric oxide elevated cGMP and decreased endothelin release, while decreased cGMP promotes endothelin release. In contrast to the inhibition of endothelin release by nitric oxide, Hirata et al. (1993) noted that endothelin promotes nitric oxide release in cultured bovine endothelial cells.
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Supports inverse NO-endothelin regulation in guinea pigs; leaves open translation to human endothelial dysfunction.
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Miller et al. (1995) studied this question.
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