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内皮对镁在去氧皮质酮盐性高血压大鼠主动脉基础张力体外血管舒张作用中的影响。

Influence of endothelium in the in vitro vasorelaxant effect of magnesium on aortic basal tension in DOCA-salt hypertensive rat.

作者信息

Laurant P, Berthelot A

机构信息

Laboratoire de Physiologie Pharmacie, UFR de Médecine et Pharmacie, Besançon, France.

出版信息

Magnes Res. 1992 Dec;5(4):255-60.

PMID:1296760
Abstract

The objective of this study was to examine the influence of the endothelium on the extracellular magnesium induced relaxation of basal tension in isolated aortas from both mineralocorticoid-salt (DOCA-salt) hypertensive and control normotensive Sprague Dawley male rats. After incubation in magnesium-free physiological salt solution (PSS) (O mM magnesium), the increase of extracellular magnesium (1.2; 4.8 mM magnesium) caused a decrease in aortic tone which was significantly greater when endothelium was disrupted. Magnesium-induced relaxation was also more pronounced when endothelial NO production was blocked by 10(-4) M N omega-nitro-L arginine methyl ester (L-NAME). It is suggested that the vasorelaxation induced by extracellular magnesium is linked to the level of aortic basal tension developed in magnesium-free PSS. The endothelium does not seem to be directly implicated in magnesium-induced vasorelaxation in aortas from normotensive rats. However, in DOCA-salt hypertensive rats, the magnesium-induced relaxation of basal tension was less in the intact aorta (though not when the endothelium was disrupted) when the cyclo-oxygenase pathway was blocked by 10(-6) M indomethacin. These data therefore suggest that extracellular magnesium can promote relaxation by endothelium-dependent and cyclo-oxygenase-dependent mechanisms such as the production of relaxing prostacyclin in isolated aorta from DOCA-salt hypertensive rats.

摘要

本研究的目的是检测内皮对细胞外镁诱导的盐皮质激素性盐(去氧皮质酮盐)高血压和对照正常血压的雄性斯普拉格-道利大鼠离体主动脉基础张力舒张的影响。在无镁生理盐溶液(PSS)(0 mM镁)中孵育后,细胞外镁(1.2;4.8 mM镁)的增加导致主动脉张力降低,当内皮被破坏时,这种降低显著更大。当内皮型一氧化氮生成被10⁻⁴ M N-ω-硝基-L-精氨酸甲酯(L-NAME)阻断时,镁诱导的舒张也更明显。提示细胞外镁诱导的血管舒张与在无镁PSS中产生的主动脉基础张力水平有关。在正常血压大鼠的主动脉中,内皮似乎未直接参与镁诱导的血管舒张。然而,在去氧皮质酮盐高血压大鼠中,当环氧化酶途径被10⁻⁶ M吲哚美辛阻断时,完整主动脉中镁诱导的基础张力舒张较小(尽管内皮被破坏时并非如此)。因此,这些数据表明细胞外镁可通过内皮依赖性和环氧化酶依赖性机制促进舒张,如在去氧皮质酮盐高血压大鼠的离体主动脉中产生舒张性前列环素。

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