生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2000年
5期
435-439
,共5页
辣椒素%最后区%平均动脉压%心率%肾交感神经活动%钌红%MK-801
辣椒素%最後區%平均動脈壓%心率%腎交感神經活動%釕紅%MK-801
랄초소%최후구%평균동맥압%심솔%신교감신경활동%조홍%MK-801
capsaicin%area postrema%mean arterial pressure%heart rate%renal sympathetic nerve activity%ruthenium red%MK-801
在36只麻醉Sprague-Dawley大鼠, 观察了最后区内微量注射辣椒素(10 μmol/L, 50 nl)对平均动脉压(MAP)、心率(HR)和肾交感神经放电(RSNA)的影响.实验结果如下:(1)最后区内注射辣椒素可引起 MAP、HR 和RSNA明显增加, 分别由12.34±0.53 kPa、 328.52±7.54 bpm 和100±0% 增至15.17±0.25 kPa (P<0.001)、 354.81±8.54 bpm (P<0.001) 和156.95±7.57% (P<0.001);(2) 静脉注射辣椒素受体阻断剂钌红(100 mmol/L, 0.2 ml) 后, 辣椒素的上述效应可被明显抑制;(3) 预先应用NMDA 受体阻断剂MK-801 (500 μg/kg, 0.2 ml, iv)也明显抑制辣椒素的兴奋效应.以上结果提示, 最后区微量注射辣椒素对血压、心率和肾交感神经放电有兴奋作用, 而此作用由辣椒素受体介导并有谷氨酸参与.
在36隻痳醉Sprague-Dawley大鼠, 觀察瞭最後區內微量註射辣椒素(10 μmol/L, 50 nl)對平均動脈壓(MAP)、心率(HR)和腎交感神經放電(RSNA)的影響.實驗結果如下:(1)最後區內註射辣椒素可引起 MAP、HR 和RSNA明顯增加, 分彆由12.34±0.53 kPa、 328.52±7.54 bpm 和100±0% 增至15.17±0.25 kPa (P<0.001)、 354.81±8.54 bpm (P<0.001) 和156.95±7.57% (P<0.001);(2) 靜脈註射辣椒素受體阻斷劑釕紅(100 mmol/L, 0.2 ml) 後, 辣椒素的上述效應可被明顯抑製;(3) 預先應用NMDA 受體阻斷劑MK-801 (500 μg/kg, 0.2 ml, iv)也明顯抑製辣椒素的興奮效應.以上結果提示, 最後區微量註射辣椒素對血壓、心率和腎交感神經放電有興奮作用, 而此作用由辣椒素受體介導併有穀氨痠參與.
재36지마취Sprague-Dawley대서, 관찰료최후구내미량주사랄초소(10 μmol/L, 50 nl)대평균동맥압(MAP)、심솔(HR)화신교감신경방전(RSNA)적영향.실험결과여하:(1)최후구내주사랄초소가인기 MAP、HR 화RSNA명현증가, 분별유12.34±0.53 kPa、 328.52±7.54 bpm 화100±0% 증지15.17±0.25 kPa (P<0.001)、 354.81±8.54 bpm (P<0.001) 화156.95±7.57% (P<0.001);(2) 정맥주사랄초소수체조단제조홍(100 mmol/L, 0.2 ml) 후, 랄초소적상술효응가피명현억제;(3) 예선응용NMDA 수체조단제MK-801 (500 μg/kg, 0.2 ml, iv)야명현억제랄초소적흥강효응.이상결과제시, 최후구미량주사랄초소대혈압、심솔화신교감신경방전유흥강작용, 이차작용유랄초소수체개도병유곡안산삼여.
The effects of capsaicin microinjection into area postrema (AP) on mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in 36 anesthetized Sprague-Dawley rats. The results obtained are as follows. (1) Following microinjection of capsaicin (10 μmol/L, 50 nl) into the AP, MAP, HR and RSNA were significantly increased from 12.34±0.53 kPa, 328.52±7.54 bpm and 100±0% to 15.17±0.25 kPa (P<0.001), 354.81±8.54 bpm (P<0.001) and 156.95±7.57% (P<0.001), respectively. (2) Ruthenium red (RR, 100 mmol/L, 0.2 ml, iv), a capsaicin receptor antagonist, significantly inhibited these effects of capsaicin. (3) Pretreatment with a NMDA receptor antagonist MK-801 (500 μg/kg, 0.2 ml, iv) also reduced these effects of capsaicin. The above results indicate that microinjection of capsaicin into AP induces excitatory effects on MAP, HR and RSNA, which are mediated by capsaicin receptors with glutamate involvement.
