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阻断大鼠延髓头端腹外侧区的血管紧张素受体可消除兴奋性血管运动紧张。

Blockade of angiotensin receptors in rat rostral ventrolateral medulla removes excitatory vasomotor tone.

作者信息

Ito S, Sved A F

机构信息

Department of Neuroscience, University of Pittsburgh, Pennsylvania 15260, USA.

出版信息

Am J Physiol. 1996 Jun;270(6 Pt 2):R1317-23. doi: 10.1152/ajpregu.1996.270.6.R1317.

Abstract

The rostral ventrolateral medulla (RVLM) plays a primary role in the tonic and phasic control of arterial blood pressure. Stimulation of angiotensin receptors in this region appears to contribute to the tonic excitatory drive of RVLM neurons involved in the control of blood pressure, but the extent of this contribution has not been previously evaluated. The present study used bilateral microinjections of angiotensin receptor antagonists into the RVLM of chloralose-anesthetized rats to determine the degree to which tonic blood pressure was dependent upon this angiotensin-mediated input. Bilateral injection into the RVLM of 1 nmol of [Sar1, Thr8]angiotensin II or [Sar1, Ile8] angiotensin II decreased blood pressure approximately 40 mmHg. The decrease in blood pressure elicited by these angiotensin antagonists was nearly as great as that elicited by complete bilateral inhibition of the RVLM produced by local injections of muscimol or elicited by inhibition of the autonomic nervous system by intravenous injection of chlorisondamine. The decrease in blood pressure caused by injection of these angiotensin antagonists was localized to the RVLM and was dose related. Responses elicited by [Sar1, Thr8]angiotensin II were eliminated by coinjection of angiotensin. In addition to markedly decreasing resting blood pressure, 1 nmol of [Sar1, Thr8]angiotensin II injected into the RVLM, also completely antagonized the increase in blood pressure elicited by blocking the tonic inhibitory influence exerted on the RVLM by neurons in the caudal ventrolateral medulla. These results demonstrate that tonic stimulation of angiotensin receptors in the RVLM accounts for much of the excitatory sympathetic vasomotor drive emanating from the RVLM.

摘要

延髓头端腹外侧区(RVLM)在动脉血压的紧张性和阶段性控制中起主要作用。刺激该区域的血管紧张素受体似乎有助于参与血压控制的RVLM神经元的紧张性兴奋驱动,但此前尚未评估这种作用的程度。本研究通过向用氯醛糖麻醉的大鼠RVLM双侧微量注射血管紧张素受体拮抗剂,以确定紧张性血压在多大程度上依赖于这种血管紧张素介导的输入。向RVLM双侧注射1 nmol的[Sar1, Thr8]血管紧张素II或[Sar1, Ile8]血管紧张素II可使血压降低约40 mmHg。这些血管紧张素拮抗剂引起的血压下降几乎与局部注射蝇蕈醇对RVLM进行完全双侧抑制或静脉注射氯异吲哚铵抑制自主神经系统所引起的血压下降一样大。注射这些血管紧张素拮抗剂所导致的血压下降局限于RVLM,且与剂量相关。[Sar1, Thr8]血管紧张素II引起的反应可通过同时注射血管紧张素而消除。除了显著降低静息血压外,向RVLM注射1 nmol的[Sar1, Thr8]血管紧张素II还完全拮抗了因阻断尾端腹外侧延髓神经元对RVLM施加的紧张性抑制作用而引起的血压升高。这些结果表明,RVLM中血管紧张素受体的紧张性刺激是RVLM发出的兴奋性交感缩血管驱动的主要原因。

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