Inhibition of ganglionic long-term potentiation decreases blood pressure in spontaneously hypertensive rats
Inhibition of ganglionic long-term potentiation decreases blood pressure in spontaneously hypertensive rats
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DOI：
10.1177/153537020122601109
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发表时间：
2001-12-01
影响因子：
3.2
通讯作者：
Hogan, YH
中科院分区：
文献类型：
--
作者：
Alkadhi, KA;Otoom, SA;Hogan, YH
交感神经节的长时程增强（Long-term potentiation of sympathetic ganglia，gLTP）是一种独特的突触可塑性形式，具有5-羟色胺依赖性，可被5-HT 3受体拮抗剂阻断。神经节传递的基础张力的长期增强（与gLTP一样）预计会导致外周阻力的持续增加，从而导致血压升高。我们研究了交感神经节中gLTP可能参与应激诱导（神经源性）高血压表达的可能性。自发性高血压大鼠（SHR）的高血压，已知对环境刺激表现出夸大的心血管防御反应，部分是由于神经源性因素。用5-HT 3受体拮抗剂托烷司琼（ICS; 5 mg/kg/天）长期治疗SHR和其血压正常的对应物Wistar京都（WKY）大鼠，导致SHR血压显著降低，但WKY大鼠血压未显著降低。累积增加ICS的日剂量（7和10 mg/kg）并未导致SHR血压显著额外降低，表明药物仅阻断SHR高血压的神经源性成分。用于间接测试从SHR切除的神经节中gLTP的存在的电生理学方法表明，gLTP先前已经在体内在这些神经节中表达。这与正常血压大鼠神经节中缺乏gLTP形成对比。结果支持gLTP对神经源性高血压表达的贡献。
Long-term potentiation of sympathetic ganglia (gLTP), a unique form of synaptic plasticity, is serotonin dependent and can be blocked with 5-HT3 receptor antagonists. Long-lasting enhancement of the basal tone of ganglionic transmission (as with gLTP) is expected to result in sustained increase in peripheral resistance that would lead to elevated blood pressure. We examined the possibility that in sympathetic ganglia, gLTP may be Involved in the expression of stress-induced (neurogenic) form of hypertension. High blood pressure in spontaneously hypertensive rat (SHR), known to show exaggerated cardiovascular defense reactions to environmental stimuli, is partly due to a neurogenic factor. Chronic treatment of SHR and their normotensive counterpart, the Wistar Kyoto (WKY) rats with the 5-HT3 receptor antagonist tropisetron (ICS; 5 mg/kg/day), caused a marked decrease in the blood pressure of the SHR but not of WKY rats. Increasing the daily dose of ICS cumulatively (7 and 10 mg/kg) did not result in significant additional decrease in blood pressure of SHR, indicating that the drug blocks only the neurogenic component of hypertension in the SHR. electrophysiological procedures for indirectly testing for the presence of gLTP in ganglia excised from SHR suggest that gLTP has been previously expressed in these ganglia in vivo. This contrasts with the absence of gLTP in ganglia from normotensive rats. The results support contribution of gLTP to the expression of neurogenic hypertension.