摘要
电击大鼠足底形成应激性高血压（ＳＩＨ），研究了缰核（Ｈｂ）在其中的作用机制。损毁Ｈｂ可降低ＳＩＨ升高的幅度。ＳＩＨ鼠内外侧Ｈｂ（ＭＨｂ，ＬＨｂ）对谷氨酸（Ｇｌｕ）的敏感性高于正常鼠。足底电击使血浆和Ｈｂ内血管紧张素Ⅱ（ＡｎｇⅡ）明显升高。侧脑室和ＭＨｂ分别注射ＡｎｇⅡ或ｓａｒａｌａｓｉｎ，在ＳＩＨ鼠引起明显的血压变化。微电泳ＡｎｇⅡ、ｓａｒａｌａｓｉｎ可分别明显改变ＳＩＨ鼠Ｈｂ内神经元的放电活动。ＡｎｇⅡ可抑制Ｈｂ细胞膜上延迟整流Ｋ＋电流（Ｉｋ）通道的活动。以同样的方法观察了Ｎ－硝基左旋精氨酸（Ｌ－ＮＮＡ）和硝普钠（ＳＮＰ）在ＳＩＨ鼠中的作用。由以上可知，电击可使Ｈｂ尤其是ＭＨｂ神经元对ＡｎｇⅡ的反应性明显增强，同时也使ＡｎｇⅡ合成增多，这些变化对于敏感化了的Ｈｂ神经元的作用更强，最终发展为ＳＩＨ。
Stress-induced hypertension (SIH) was performed by electric shock on hind paw in rats. Habenula(Hb) lesion decreased the degree of SIH. After stress, the AngⅡ concentration in blood plasma and in Hb were increased. BP was elevated after icv or MHb administration of AngⅡ, and decreased after microinjection of saralasin into MHb. The BP changes induced by AngⅡ and saralasin were more prominent in SIH than in normotensive rats. Iontophoresis of AngII (or saralasin) into Hb increased (or decreased) the discharges of the excitatory neurons related to cardiovascular activity. AngⅡ could inhibit the activity of Ik channel. Using the same methods, the actions of LNNA and SNP were investigated. From above, it is suggested that Hb is involved in the development of SIH. Stress stimulus strengthened the sensitivity of Hb, especially MHb to AngⅡ, and also induced an increase of AngII. These changes would promote the response of sensitized Hb in the development of SIH.
出处
《生理科学进展》
CAS
CSCD
北大核心
1998年第3期231-234,共4页
Progress in Physiological Sciences
关键词
缰核
应激性高血压
血管紧张素Ⅱ
硝普钠
钾通道
Habenula nucleus
Stress-induced hypertension
AngiotensinII
Saralasin
SNP
Ik channel
