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实验观察了侧脑室注射 (icv)及缰核 (habenulanucleusHb)内微电泳血管紧张素Ⅱ (AⅡ )与 [Sar1,Thr8] AⅡ (ST AⅡ ,AⅡ拮抗剂 )对正常和应激性高血压 (stress inducedhypertensionSIH)大鼠血压及内外侧缰核 (MHb、LHb)内心血管神经元放电活动的影响。结果如下 :icvAⅡ或ST AⅡ ,正常鼠和SIH大鼠血压均升高或降低 ,SIH鼠较正常鼠血压变化更显著 (P <0 0 5 ) ;icvAⅡ或微电泳AⅡ明显增强Hb内心血管神经元的放电活动 ,对SIH大鼠作用更明显 ;而微电泳ST AⅡ则明显抑制Hb内心血管神经元的放电活动 ,对SIH大鼠的抑制作用更强。研究表明 :中枢内AⅡ参与SIH的形成 ,SIH大鼠Hb内心血管神经元对AⅡ反应的敏感性提高了。
The effects of angiotensin Ⅱ (AⅡ) and [Sar1, Thr8] AⅡ (ST AⅡ, AⅡ antagonist) on the expression of angiotensin Ⅱ in normal and stress hypertension (icv) and habenulanucleusHb induced hyperthyroidism in rats and the discharge activity of cardiovascular neurons in the medial and lateral habenular nucleus (MHb, LHb). The results were as follows: icvAⅡ or ST AⅡ, the blood pressure of normal rats and SIH rats were all increased or decreased, the changes of blood pressure of SIH rats were more significant than that of normal rats (P <0.05); icvAⅡ or AⅡ of microelectrophoresis significantly enhanced cardiovascular neurons Of discharge activity, the effect on SIH rats is more obvious; while micro-electrophoresis ST A Ⅱ significantly inhibit the discharge activity of Hb cardiovascular neurons, the inhibition of SIH rats stronger. Studies have shown that central AⅡ is involved in the formation of SIH, and cardiovascular neurons in HH of SIH rats are more sensitive to AⅡ response.