VENTROLATERAL MEDULLA IN SPONTANEOUSLY HYPERTENSIVE RATS - ROLE OF ANGIOTENSIN-II
VENTROLATERAL MEDULLA IN SPONTANEOUSLY HYPERTENSIVE RATS - ROLE OF ANGIOTENSIN-II
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DOI：
10.1152/ajpregu.1993.264.2.r388
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发表时间：
1993-02-01
影响因子：
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通讯作者：
AVERILL, DB
中科院分区：
文献类型：
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作者：
MURATANI, H;FERRARIO, CM;AVERILL, DB
我们研究了自发性高血压大鼠（SHR）和血压正常的Wistar-Kyoto（WKY）大鼠延髓腹外侧区（VLM）内源性血管紧张素II（ANG II）是否参与心血管调节。通过将100 pmol [Sar 1，Thr 8]ANG II微量注射到吻侧（R）或尾侧（C）VLM中，检查VLM内源性ANG II的作用。这种ANG II拮抗剂引起RVLM的降压和心动过缓反应，以及CVLM的升压和心动过速反应。SHR的血压反应幅度（RVLM为-27 +/-3 mmHg，CVLM为29 +/-4 mmHg）显著大于WKY大鼠（分别为-17 +/-1和17 +/-2 mmHg）（RVLM为P < 0.01，CVLM为P < 0.05）。双侧注射蝇蕈醇抑制RVLM神经元的紧张性活动表明，血管紧张素Ⅱ拮抗剂注射在CVLM产生的升压反应，需要完整的嘴侧升压神经元。目前的数据表明，血管紧张素Ⅱ内源性RVLM和CVLM作为紧张性兴奋剂对VLM的血管神经元。当以血压的变化来衡量血管紧张素Ⅱ阻断的效果时，SHR的RVLM和CVLM中的血管紧张素Ⅱ对血压水平的贡献显著大于WKY大鼠（P < 0.01）。RVLM中γ-氨基丁酸（GABA）A受体的阻断表明，在该菌株中，对RVLM的抑制性GABA能输入并未减少。ANG Ⅱ在SHR RVLM的作用增强可能与RVLM神经元的高紧张性活动有关，而其在CVLM的作用可能与RVLM的抑制性输入有关。然而，这种抑制可能不足以抵消SHR RVLM神经元明显更大的内在升压活性。
We investigated whether angiotensin II (ANG II), endogenous to the ventrolateral medulla (VLM), contributes to cardiovascular regulation in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. The action of ANG II endogenous to the VLM was examined by microinjection of 100 pmol of [Sar1, Thr8]ANG II into either the rostral (R) or caudal (C) VLM. This ANG II antagonist caused depressor and bradycardic responses in the RVLM and pressor and tachycardic responses in the CVLM. The magnitude of the blood pressure responses was significantly greater (P < 0.01 in RVLM and P < 0.05 in CVLM) in SHRs (-27 +/- 3 mmHg in RVLM and 29 +/-4 mmHg in CVLM) than in WKY rats (-17 +/- 1 and 17 +/- 2 mmHg, respectively). Suppression of tonic activity of RVLM neurons by bilateral injection of muscimol in the RVLM showed that the pressor response produced by ANG II antagonist injection in the CVLM required the integrity of rostral pressor neurons. The present data suggest that ANG II endogenous to RVLM and CVLM acts as a tonic excitatory agent on vasomotor neurons of the VLM. The contribution of ANG II in the RVLM and CVLM to the prevailing level of blood pressure was significantly (P < 0.01) larger in SHRs vs. WKY rats when the effect of ANG II blockade was measured as the change in blood pressure. Blockade of gamma-aminobutyric acid (GABA)A receptors in the RVLM showed that inhibitory GABAergic input to the RVLM was not diminished in this strain. The increased action of ANG II in the RVLM of SHR may relate to a higher tonic activity of RVLM neurons, whereas its action in the CVLM may contribute to the inhibitory input to the RVLM. However, this inhibition may not be sufficient to counterbalance the apparent greater intrinsic pressor activity of RVLM neurons of SHRs.