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高盐饮食对Sprague-Dawley大鼠孤束核中γ-氨基丁酸介导反应的影响。

Effect of a high-salt diet on gamma-aminobutyric acid-mediated responses in the nucleus tractus solitarius of Sprague-Dawley rats.

作者信息

Masubuchi Yuichi, Tsukamoto Kazuyoshi, Isogai Osamu, Yajima Yoshiharu, Ito Satoru, Saito Satoshi, Uchiyama Takahisa

机构信息

Second Department of Internal Medicine, Nihon University School of Medicine, 30-1, Oyaguchi-Kamichou, Itabashi-ku, Tokyo 173-8610, Japan.

出版信息

Brain Res Bull. 2004 Sep 30;64(3):221-6. doi: 10.1016/j.brainresbull.2004.07.009.

Abstract

Previous study using an indirect gamma-aminobutyric acid (GABA) agonist indicated that high salt intake enhances sensitivity of nucleus tractus solitarius (NTS) projecting inhibitory input to rostral ventrolateral medulla sympathoexcitatory neurons. We further investigated the relationship between salt intake and the GABA system in NTS. Sprague-Dawley (S-D) rats consuming high dietary salt (8%) or low dietary salt (0.3%) for 3 weeks were used. Under chloralose-anesthesia, baseline arterial pressure (AP) and heart rate (HR) were similar in both groups. Bilateral injection into NTS of nipecotic acid, GABA(A) receptor agonist (muscimol), or GABA(B) receptor agonist (baclofen) elicited greater pressor responses in high-salt group. GABA(A) receptor antagonist, bicuculline and GABA(B) receptor antagonist, CGP-35348 elicited greater depressor responses. Phenylephrine or nitroprusside (i.v.) elicited similar respective increases or decreases in AP in both groups. Baroreflex sensitivity was similar. Thus, high-salt intake enhances both GABA(A) receptor- and GABA(B) receptor-mediated responses within NTS, thereby inhibiting elevation of AP.

摘要

先前使用间接γ-氨基丁酸(GABA)激动剂的研究表明,高盐摄入会增强孤束核(NTS)向延髓头端腹外侧交感兴奋神经元投射的抑制性输入的敏感性。我们进一步研究了盐摄入与NTS中GABA系统之间的关系。使用了食用高盐饮食(8%)或低盐饮食(0.3%)3周的Sprague-Dawley(S-D)大鼠。在氯醛糖麻醉下,两组的基线动脉压(AP)和心率(HR)相似。向NTS双侧注射烟酸、GABA(A)受体激动剂(蝇蕈醇)或GABA(B)受体激动剂(巴氯芬)在高盐组中引起更大的升压反应。GABA(A)受体拮抗剂荷包牡丹碱和GABA(B)受体拮抗剂CGP-35348引起更大的降压反应。去氧肾上腺素或硝普钠(静脉注射)在两组中分别引起相似的AP升高或降低。压力感受性反射敏感性相似。因此,高盐摄入增强了NTS内GABA(A)受体和GABA(B)受体介导的反应,从而抑制了AP的升高。

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