Excitatory amino acids in the rostral ventrolateral medulla support blood pressure in spontaneously hypertensive rats
Excitatory amino acids in the rostral ventrolateral medulla support blood pressure in spontaneously hypertensive rats
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DOI：
10.1161/01.hyp.35.1.413
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发表时间：
2000-01-01
期刊：
影响因子：
8.3
通讯作者：
Sved, AF
中科院分区：
文献类型：
--
作者：
Ito, S;Komatsu, K;Sved, AF
将兴奋性氨基酸（EAA）拮抗剂犬尿烯酸（KYN）注入麻醉大鼠延髓头端腹外侧区（RVLM）对动脉压无影响。然而，我们最近报道，在抑制延髓尾侧腹外侧区后，将KYN注射到RVLM使动脉压降低到与完全抑制RVLM所产生的相同水平。我们已经表明，这些结果反映了紧张性活性EAA介导的输入RVLM产生直接兴奋RVLM血管神经元和间接抑制这些神经元。在此模型的基础上，我们假设这些EAA驱动的直接兴奋和间接抑制的影响之间的平衡RVLM可能会改变实验性高血压模型。为了开始验证这一假设，比较了自发性高血压大鼠（SHR）和Wistar-Kyoto大鼠（WKY）的RVLM中注射KYN的作用。在氯醛糖麻醉的WKY，双侧注射KYN到RVLM没有改变动脉压，而类似的注射在SHR平均动脉压降低约40毫米汞柱。抑制后的尾侧腹外侧髓质，这同样增加了两个菌株的动脉压，注射KYN到RVLM降低平均动脉压的水平，产生自主神经阻滞。这些结果表明，兴奋性和抑制性影响的平衡RVLM血管神经元驱动的紧张性活性EAA介导的输入RVLM在SHR中被破坏，并可能有助于在SHR的高血压。
Injection of the excitatory amino acid (EAA) antagonist kynurenic acid (KYN) into the rostral ventrolateral medulla (RVLM) of anesthetized rats has no effect on arterial pressure. However, we recently reported that after inhibition of the caudal ventrolateral medulla, injection of KYN into the RVLM decreased arterial pressure to the same level as produced by complete inhibition of the RVLM. We have suggested that these results reflect tonically active EAA-mediated inputs to the RVLM producing both direct excitation of RVLM vasomotor neurons and indirect inhibition of these neurons. On the basis of this model, we hypothesize that the balance between these EAA-driven direct excitatory and indirect inhibitory influences on the RVLM may be altered in models of experimental hypertension. To begin to test this hypothesis, the effects of injecting KYN into the RVLM of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were compared. In chloralose-anesthetized WKY, bilateral injection of KYN into the RVLM did not alter arterial pressure, whereas similar injections in SHR reduced mean arterial pressure by approximate to 40 mm Hg. After inhibition of the caudal ventrolateral medulla, which similarly increased arterial pressure in both strains, injection of KYN into the RVLM reduced mean arterial pressure to the same level as produced by autonomic blockade. These results suggest that the balance of excitatory and inhibitory influences on RVLM vasomotor neurons driven by tonically active EAA-mediated inputs to the RVLM is disrupted in SHR and may contribute to the hypertension in SHR.