Fig. 4

Cx37 is implicated in basal NO release. Aortic segments obtained from WT, Cx37^−/−, Cx40^−/− or Cx40^+/− mice were mounted in a wire-myograph and concentration-response curves for PHE were generated in presence or absence of L-NAME (100 μM). a Inhibition of NO synthesis by L-NAME increased the contractile amplitude for PHE in WT aortas indicating presence of basal NO release. This effect of L-NAME was not observed in aortas isolated from Cx37^−/− (b) or Cx40^−/− (c) mice. In contrast (d), in aortas obtained from Cx40^+/− mice L-NAME did increase the contractile amplitude of PHE. Values are expressed as mean ± SEM. N = 6–10. **, *** p < 0.01, 0.001 vs control, respectively. e Representative image and quantification of eNOS protein expression in protein samples from scraped mouse aortic endothelial cells as assessed by western blot. Values are expressed as mean ± SEM. N = 6–8. * p < 0.05 vs WT