Ex vivo study of the effects of dietary magnesium deficiency on the formation and release of NO from endothelial cells and the sensitivity to NO of smooth muscle cells of thoracic aortas isolated from rats.

We found that the contractile responses to phenylephrine (PE) of isolated endothelium-intact thoracic aortas were enhanced by a nitric oxide (NO) synthase inhibitor, nitro-L-arginine (LNAG). and the magnitude of this enhancement was significantly greater in Mg-deficient than control rats. In this study, we used a sandwich method to evaluate the effects of dietary Mg deficiency on the ability of vascular endothelial cells to form and/or release NO and on the sensitivity to NO of vascular smooth muscle cells. Male Wistar rats were fed a Mg-deficient (10 mg Mg/kg diet) or control (700 mg Mg/kg diet) diet for 30 days. With the sandwich method, when endothelium-denuded thoracic aortas from chow fed rats were used as the assay vessels, and endothelium-intact aortas from control or Mg-deficient rats were used as the NO-donor vessels, neither the aortic contractile responses to PE nor the enhancement by LNAG of these responses in control and Mg-deficient rats differed significantly. When endothelium-denuded thoracic aortas from control or Mg deficient rats were used as the assay vessels and endothelium-intact aortas from chow fed rats were used as NO-donor vessels, LNAG enhanced PE-induced contractions to a significantly greater extent in Mg-deficient than control rats. Furthermore, sodium nitroprusside (a NO donor) had a greater relaxant effect on endothelium-denuded thoracic aortas isolated from Mg-deficient than control rats. These ex vivo results suggest that dietary Mg deficiency in rats has little effect on the formation and/or release of NO by aortic endothelial cells. but it does appear to increase the sensitivity to NO of aortic smooth muscle cells.