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正常血压和自发性高血压大鼠延髓中谷氨酸能对[3H]-去甲肾上腺素释放的调节作用。

Glutamatergic regulation of [3H]-noradrenaline release in the medulla oblongata of normotensive and spontaneously hypertensive rats.

作者信息

Tsuda K, Tsuda S, Nishio I, Masuyama Y, Goldstein M

机构信息

Department of Medicine, Wakayama Medical College, Japan.

出版信息

J Hypertens. 1994 May;12(5):517-22.

PMID:7930551
Abstract

OBJECTIVE

To assess in vitro the role of glutamate receptors in the regulation of noradrenaline release from the medulla oblongata of normotensive and hypertensive rats.

DESIGN AND METHODS

The effects of L-glutamate (an endogenous ligand for glutamate receptors), glycine (an allosteric agonist for the N-methyl-D-aspartate type of glutamate receptors) and MK-801 (an antagonist for N-methyl-D-aspartate receptors) on [3H]-noradrenaline release were examined in slices of rat medulla oblongata.

RESULTS

L-Glutamate elicited [3H]-noradrenaline release from slices of rat medulla oblongata in magnesium-free medium. Glycine also increased the release of noradrenaline. Moreover, the effect of L-glutamate on noradrenaline release was significantly potentiated by glycine. MK-801 inhibited the increase in noradrenaline release evoked by L-glutamate. In spontaneously hypertensive rats (SHR) the facilitatory effect of L-glutamate on noradrenaline release was significantly more pronounced than in Wistar-Kyoto (WKY) rats. Furthermore, glycine alone and in combination with L-glutamate increased the noradrenaline release to a greater extent in SHR than in WKY rats.

CONCLUSION

The present results show that the excitatory amino acids might increase noradrenaline release from rat medulla oblongata, which was partially dependent on the N-methyl-D-aspartate type of glutamate receptors. The greater effect of L-glutamate and glycine in SHR suggests that these amino acids might be involved in the regulation of noradrenaline release in the medulla oblongata of hypertension.

摘要

目的

在体外评估谷氨酸受体在正常血压和高血压大鼠延髓去甲肾上腺素释放调节中的作用。

设计与方法

在大鼠延髓切片中检测L-谷氨酸(谷氨酸受体的内源性配体)、甘氨酸(N-甲基-D-天冬氨酸型谷氨酸受体的变构激动剂)和MK-801(N-甲基-D-天冬氨酸受体拮抗剂)对[3H]-去甲肾上腺素释放的影响。

结果

在无镁培养基中,L-谷氨酸可引起大鼠延髓切片释放[3H]-去甲肾上腺素。甘氨酸也增加去甲肾上腺素的释放。此外,甘氨酸可显著增强L-谷氨酸对去甲肾上腺素释放的作用。MK-801可抑制L-谷氨酸引起的去甲肾上腺素释放增加。在自发性高血压大鼠(SHR)中,L-谷氨酸对去甲肾上腺素释放的促进作用比Wistar-Kyoto(WKY)大鼠更为明显。此外,单独使用甘氨酸以及甘氨酸与L-谷氨酸联合使用时,SHR中去甲肾上腺素的释放增加程度比WKY大鼠更大。

结论

目前的结果表明,兴奋性氨基酸可能增加大鼠延髓去甲肾上腺素的释放,这部分依赖于N-甲基-D-天冬氨酸型谷氨酸受体。L-谷氨酸和甘氨酸在SHR中的作用更强,表明这些氨基酸可能参与高血压大鼠延髓去甲肾上腺素释放的调节。

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