Sakaguchi H, Ishiguro S, Miyamoto A, Nishio A
Department of Veterinary Pharmacology, Faculty of Agriculture, Kagoshima University, Japan.
Magnes Res. 1994 Dec;7(3-4):199-206.
The present study was undertaken to examine whether the enhanced contractile response to phenylephrine observed in thoracic aorta isolated from dietary magnesium-deficient rats depends on an increased density of alpha 1-adrenoceptor or calcium channels. Adult male Wistar rats were fed with a magnesium-deficient diet (0.001 per cent magnesium) for 30 days with control groups (0.07 per cent magnesium). The contractile response to phenylephrine was significantly inhibited by nifedipine in both aortas without endothelium, and the degree of the inhibition was significantly greater in magnesium-deficient rats than in controls. Membranes were isolated from both thoracic aortas without endothelium, and the binding of [3H]PN200-110 or [3H]prazosin to the membranes was studied. A single binding site for [3H]PN200-110 or [3H]prazosin was evident for both membranes with high affinity. Dietary magnesium-deficiency increased significantly the maximal number (Bmax) of [3H]PN200-110 binding sites, but not Bmax of [3H]prazosin, and did not alter the binding affinity of both ligands. These results suggest that increased density of calcium channels participates in the enhanced contractile response to phenylephrine in thoracic aortas isolated from dietary magnesium-deficient rats.
本研究旨在探讨从饮食缺镁大鼠分离的胸主动脉中观察到的对去氧肾上腺素收缩反应增强是否取决于α1 -肾上腺素能受体或钙通道密度的增加。成年雄性Wistar大鼠用缺镁饮食(0.001%镁)喂养30天,对照组用正常饮食(0.07%镁)。在无内皮的主动脉中,硝苯地平显著抑制了对去氧肾上腺素的收缩反应,且缺镁大鼠的抑制程度显著大于对照组。从无内皮的胸主动脉中分离出细胞膜,并研究了[3H]PN200 - 110或[3H]哌唑嗪与细胞膜的结合。两种细胞膜对[3H]PN200 - 110或[3H]哌唑嗪均有一个具有高亲和力的单一结合位点。饮食缺镁显著增加了[3H]PN200 - 110结合位点的最大数量(Bmax),但未增加[3H]哌唑嗪的Bmax,且未改变两种配体的结合亲和力。这些结果表明,钙通道密度增加参与了从饮食缺镁大鼠分离的胸主动脉中对去氧肾上腺素收缩反应的增强。