摘要
雄性Sprague-Dawey大鼠,用乌拉坦(70mg/kg)和氯醛糖(30mg/kg)腹腔麻醉。在双侧头端延髓腹外侧区(rVLM区)每侧微量注射血管加压素(AVP)(10pmol/o.1μl)可引起平均动脉压(MBP)升高,心率(HR)变化不明显,每侧微量注射AVP的V1受体拮抗利d(CH2)5[Tyr(Me)2]AVP(0.1nmol/0.1μl)后MBP和HR无明显变化。若预先在rVLM区每侧微量注射AVP的V1受体拮抗剂(0.1nmol/0.1μl)后,再在rVLM区同一部位每侧注入AVP(10pmol/0.1μl),MBP升高作用消失。电刺激中脑(dPAG区)可诱发防御性升压反应。若在双侧rYLM区每侧微量注射AVP的V1受体拮抗剂(0.1nmol/0.1μl)可对防御性升压反应起部分抑制作用。结果表明,rVLM区内微量注射AVP可引起MBP升高,刺激中脑dPAG区诱发的升压反应均与rVLM区AVP的V1受体的激活有关。
Experiments were Performed on male SD rats anaesthetized with urethane(700 mg/kg) and chloralose(35 mg/kg). The results showed that mean arterial pressure(MBP)increased signifigantly and heart rate (HR) had no signifigant change by bilateral microinjection AVP(10 pmol/0. 1 μl/site) into the rostral ventrolateral medulla(rVLM ),while both MBP and HR were not changed by application of an AVP-Vl receptor antagnoist. Microinjection of an AVP-Vl receptor antagonist into the bilateral rVLM inhibited partially the pressor response induced by midbrain defence area stimulation. The above results suggest that AVP in the rVLM can elevate MBP and midbrain defence area stimulation can cause pressor resPonse. Both these effects are related to activation of AVP-V1 receptos in the rVLM.
出处
《生理学报》
CAS
CSCD
北大核心
1997年第5期491-496,共6页
Acta Physiologica Sinica
基金
国家自然科学基金!39270815