延髓头端腹外侧区血管升压素能机制在应激性高血粘度中的作用

AVP-ergic mechanism in the rostral ventrolateral medulla: a possible role in stress induced hyperviscosity

观察延髓头端腹外侧区 (rVLM)微量注射血管升压素 (AVP)能否影响正常大鼠的血压和血粘度 ,并分析rVLM内AVP能机制在清醒大鼠经悬吊加束缚引起应激性升压反应和高血粘度中的影响。结果如下 :(1)正常大鼠双侧rVLM微量注射AVP (每侧 0 5 μg/0 5 μl) ,可引起血压和血粘度升高 ;此作用可被事先在同一位置微量注射AVP V1受体拮抗剂d(CH2 ) 5[Tyr(Me) 2 ]AVP(每侧 0 1μg/0 5 μl)所阻断。 (2 )束缚大鼠双侧rVLM等量注射AVP V1受体拮抗剂可降低束缚大鼠引起的高血粘度和血压升高。但不能被双侧延髓尾端腹外侧区 (cVLM) ,或静脉内等量注射AVP V1受体拮抗剂所阻断 ,也不能被双侧rVLM等量注射AVP V2 受体拮抗剂 [adamantaneacetyl1,O Et D Tyr2 ,Val4 ,aminobutyryl6,Arg8,9] vasopressin (每侧 0 1μg/0 5 μl)所阻断。上述结果表明 :rVLM内AVP能受体激活可参与rVLM内注入AVP引起的血压和血粘度升高或束缚诱发的应激性升压反应和高血粘度。

The study was undertaken to find whether microinjection of vasopressin (AVP) into the rostral ventrolateral medulla (rVLM) affects blood pressure (BP) and blood viscosity in rats and to analyze the effects of AVP ergic mechanism in the rVLM on stress induced hyperviscosity of rats. The results are as follows. (1) Microinjection of AVP into the rostral ventrolateral medulla (rVLM) of normal rats resulted in a significant increase in BP and plasma viscosity, which was blocked by bilateral microinjection of AVP V 1 receptor antagonist (d(CH 2) 5[Tyr(Me) 2]AVP) into the same area. (2) The stress induced pressor response and hyperviscosity was abolished by microinjection of AVP V 1 receptor antagonist into the rVLM, but not by AVP V 2 receptor antagonist ([adamantaneacetyl 1,O Et D Tyr 2,Val 4,aminobutyryl 6,Arg 8,9 ] vasopressin). Micro^in^jec^tion of AVP V 1 receptor antagonist of the same dosage into bilateral caudal ventrolateral medulla (cVLM) or intravenous injection of the antagonist of the same dosage had no effect. The above results suggest that the increase of BP and plasma viscosity induced by microinjection of AVP into rVLM and the stress induced pressor response and hyperviscosity caused by restraining may be mediated by activation of the AVP V 1 receptor in the rVLM.