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GABAA和GABAB受体在大鼠延髓头端腹外侧区血压的紧张性抑制调控中的作用。

Involvement of both GABAA and GABAB receptors in tonic inhibitory control of blood pressure at the rostral ventrolateral medulla of the rat.

作者信息

Amano M, Kubo T

机构信息

Department of Pharmacology, Showa College of Pharmaceutical Sciences, Tokyo, Japan.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1993 Aug;348(2):146-53. doi: 10.1007/BF00164791.

Abstract

The rostral ventrolateral medulla (RVLM) contains vasopressor neurons which increase vasomotor tone. Endogenous GABA is suggested to be involved in mediation of the tonic inhibition of vasopressor neurons in the RVLM. To obtain more precise information about GABAergic mechanisms in the RVLM, we microinjected GABA agonists and antagonists unilaterally into the RVLM and examined their effects on blood pressure and heart rate. In addition, involvement of the other inhibitory amino acids glycine, beta-alanine and taurine in blood pressure regulation in the rat RVLM was also investigated. Male Wistar rats were anesthetized with urethane, paralyzed and artificially ventilated. The GABAA agonist muscimol (3-30 pmol) and the GABAB agonist baclofen (10-100 pmol) microinjected into the RVLM produced a decrease in blood pressure. The GABAA antagonist bicuculline (300 pmol) abolished the depressor response to muscimol (10 pmol) but not to baclofen (30 pmol) whereas the GABAB antagonist 2-hydroxysaclofen (1 nmol) abolished the depressor response to baclofen (30 pmol) but not to muscimol (10 pmol). Either bicuculline or 2-hydroxysaclofen alone produced a pressor response. Both antagonists inhibited depressor responses to nipecotic acid (7.7 nmol) and GABA (0.3 nmol). Glycine (0.13-4.0 nmol), beta-alanine (0.11-3.4 nmol) and taurine (0.08-2.4 nmol) microinjected into the RVLM also produced decreases in blood pressure. The glycine antagonist strychnine (0.58 nmol) abolished the depressor response to glycine, beta-alanine and taurine but not to GABA. The taurine antagonist 6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine-1,1-dioxide) (1.3 nmol) inhibited the depressor response to beta-alanine and taurine but not to glycine and GABA.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

延髓头端腹外侧区(RVLM)含有能增强血管运动张力的升压神经元。内源性γ-氨基丁酸(GABA)被认为参与介导RVLM中升压神经元的紧张性抑制。为了获取关于RVLM中GABA能机制的更精确信息,我们将GABA激动剂和拮抗剂单侧微量注射到RVLM中,并检测它们对血压和心率的影响。此外,还研究了其他抑制性氨基酸甘氨酸、β-丙氨酸和牛磺酸在大鼠RVLM血压调节中的作用。雄性Wistar大鼠用乌拉坦麻醉、麻痹并进行人工通气。向RVLM中微量注射GABAA激动剂蝇蕈醇(3 - 30皮摩尔)和GABAB激动剂巴氯芬(10 - 100皮摩尔)可使血压降低。GABAA拮抗剂荷包牡丹碱(300皮摩尔)消除了对蝇蕈醇(10皮摩尔)的降压反应,但未消除对巴氯芬(30皮摩尔)的降压反应,而GABAB拮抗剂2-羟基-巴氯芬(1纳摩尔)消除了对巴氯芬(30皮摩尔)的降压反应,但未消除对蝇蕈醇(10皮摩尔)的降压反应。单独使用荷包牡丹碱或2-羟基-巴氯芬均可产生升压反应。两种拮抗剂均抑制了对尼克酸(7.7纳摩尔)和GABA(0.3纳摩尔)的降压反应。向RVLM中微量注射甘氨酸(0.13 - 4.0纳摩尔)、β-丙氨酸(0.11 - 3.4纳摩尔)和牛磺酸(0.08 - 2.4纳摩尔)也可使血压降低。甘氨酸拮抗剂士的宁(0.58纳摩尔)消除了对甘氨酸、β-丙氨酸和牛磺酸的降压反应,但未消除对GABA的降压反应。牛磺酸拮抗剂6-氨甲基-3-甲基-4H-1,2,4-苯并噻二嗪-1,1-二氧化物(1.3纳摩尔)抑制了对β-丙氨酸和牛磺酸的降压反应,但未抑制对甘氨酸和GABA的降压反应。(摘要截取自250词)

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