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. 2012 Jul 5;3:128. doi: 10.3389/fphar.2012.00128

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Copyright © 2012 Costell, Ancellin, Bernard, Zhao, Upson, Morgan, Maniscalco, Olzinski, Ballard, Herry, Grondin, Dodic, Mirguet, Bouillot, Gellibert, Coatney, Lepore, Jucker, Jolivette, Willette, Schnackenberg and Behm.

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Direct vasodilatory effects of various NO/sGC/cGMP pathway modulators in aorta isolated from ND and HSFD SHR-SP. (A) As compared to ND SHR-SP, the maximal vasodilatory response to carbachol, an endothelium- and NO-dependent vasodilator, was suppressed in HSFD SHR-SP. (B) The vasodilatory response to the endothelium-independent vasodilator and NO-donor SNP was also inhibited in HSFD SHR-SP, being right-shifted 3.5-fold as compared to the response observed in ND animals. In contrast to the blunted vasodilatory responses seen with the NO-dependent vasodilators carbachol and SNP, chronic HSFD did not alter the direct vasodilatory effects of (C) the sGC stimulator BAY 60-4552 or (D) the sGC activator GSK2181236A. All data are mean ± SEM of 8–14 animals. Statistical comparisons of vasodilatory pEC₅₀ and E_max values are provided in Table 3.