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目的 :探讨缰核中的一氧化氮 ( NO)是否参与应激性高血压的形成。方法 :观察由侧脑室注射左旋硝基精氨酸 ( L- NNA)和硝普钠 ( SNP)对血压和缰核内心血管兴奋性神经元电活动的影响。结果 :SNP( 1 0μg)使应激性高血压大鼠血压的下降幅度大于正常鼠 ( P<0 .0 5 ) ;L - NNA( 2 0μg)对应激性高血压大鼠缰核外侧面 ( LHb)心血管兴奋性神经元的兴奋作用低于正常鼠 ,对应激性高血压大鼠缰核内侧面 ( MHb)心血管兴奋性神经元的兴奋作用明显。结论 :缰核内的心血管兴奋性神经元 NO通路调节心血管活动过程 ,缰核内的 NO通路可能参与应激性高血压的形成
Objective: To investigate whether nitric oxide (NO) in the habenula is involved in the formation of stress-induced hypertension. Methods: The effects of L-NNA and SNP on the blood pressure and the activity of cardiovascular excitatory neurons in the habenula were observed. Results: SNP (10 μg) decreased the blood pressure of stress - induced hypertensive rats more than that of normal rats (P <0.05); L - NNA (20 μg) LHb) excitatory activity of cardiovascular excitatory neurons is lower than that of normal mice, and excitatory effects on cardiovascular excitatory neurons of medial side (MHb) of habenula in stress-induced hypertensive rats are obvious. CONCLUSION: The NO pathway of cardiovascular excitatory neurons in the habenular nucleus regulates the cardiovascular activity. The NO pathway in the habenula may be involved in the formation of stress-induced hypertension