Journal of the American College of Nutrition · 2004
In vitro application of endotoxin to thoracic aortas from magnesium-deficient rats enhances vascular hyporeactivity to phenylephrine.
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Miyamoto Atsushi, Moriki Hiroshi, Ishiguro Shigeru, Nishio Akira
Аннотация
OBJECTIVE: Endotoxin-induced vascular hyporeactivity to phenylephrine (PE) is well described in rat aortas, but has not been investigated in those from magnesium (Mg)-deficient rats in vitro.
METHODS: Segments of thoracic aorta from control and Mg-deficient rats were incubated in culture medium for 6 hours in the presence or absence of bacterial lipopolysaccharide (LPS; 0.001-10 microg/mL). Contractions to PE were measured with or without an inducible nitric oxide synthase (iNOS) inhibitor (1400W; 0.1 and 1 microM), a guanylate cyclase inhibitor (ODQ; 0.1 and 1 microM), or a potassium channel inhibitor (TEA; 1 and 10 mM).
RESULTS: LPS induced hyporeactivity in a concentration-dependent manner under relatively low concentrations (0.001-0.1 microg/mL), however, there was no significant difference at 0.1, 1 and 10 microg/mL. LPS-induced hyporeactivity was not significantly affected by endothelium-denudation. The hyporeactivity was enhanced in thoracic aortas from Mg-deficient rats by LPS (0.01, 0.1 and 1 microg/mL). LPS (1 microg/mL) induced hyporeactivity was reversed with 1400W, ODQ or TEA in both aortas in a concentration-dependent manner, however the degree of reversal was weaker in the Mg-deficient rat aorta than in the control rat one. iNOS mRNA level was increased by LPS (0.1 microg/mL) and the increment was significantly high in Mg-deficient rat thoracic aorta.
CONCLUSIONS: From these results it is clearly demonstrated that LPS-induced vascular hyporeactivity to PE is enhanced in thoracic aorta from Mg-deficient rats, and it is suggested that LPS-induced NO production might contribute to the enhancement via stimulation of NO-cyclic GMP-potassium channel pathway.
METHODS: Segments of thoracic aorta from control and Mg-deficient rats were incubated in culture medium for 6 hours in the presence or absence of bacterial lipopolysaccharide (LPS; 0.001-10 microg/mL). Contractions to PE were measured with or without an inducible nitric oxide synthase (iNOS) inhibitor (1400W; 0.1 and 1 microM), a guanylate cyclase inhibitor (ODQ; 0.1 and 1 microM), or a potassium channel inhibitor (TEA; 1 and 10 mM).
RESULTS: LPS induced hyporeactivity in a concentration-dependent manner under relatively low concentrations (0.001-0.1 microg/mL), however, there was no significant difference at 0.1, 1 and 10 microg/mL. LPS-induced hyporeactivity was not significantly affected by endothelium-denudation. The hyporeactivity was enhanced in thoracic aortas from Mg-deficient rats by LPS (0.01, 0.1 and 1 microg/mL). LPS (1 microg/mL) induced hyporeactivity was reversed with 1400W, ODQ or TEA in both aortas in a concentration-dependent manner, however the degree of reversal was weaker in the Mg-deficient rat aorta than in the control rat one. iNOS mRNA level was increased by LPS (0.1 microg/mL) and the increment was significantly high in Mg-deficient rat thoracic aorta.
CONCLUSIONS: From these results it is clearly demonstrated that LPS-induced vascular hyporeactivity to PE is enhanced in thoracic aorta from Mg-deficient rats, and it is suggested that LPS-induced NO production might contribute to the enhancement via stimulation of NO-cyclic GMP-potassium channel pathway.