Brain histamine regulates pressor responses to peripheral hyperosmolality.
Brain histamine regulates pressor responses to peripheral hyperosmolality.
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脑组胺调节对外周高渗透压的升压反应。
DOI：
10.1152/ajpregu.1990.259.3.r507
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Bealer,SL
中科院分区：
文献类型：
--
作者：
Akins,VF;Bealer,SL
在清醒的Sprague-Dawley大鼠上研究了脑组织组胺（HA）在外周高渗性升压反应中的作用。在30分钟高渗盐水（HTS; 10微升.100 g体重-1 x min-1）静脉输注期间，在溶剂处理对照组（20.1 +/- 3.8 mmHg）和用特异性H2-拮抗剂西咪替丁进行中枢预处理的动物（15.0 +/- 3.7 mmHg）中观察到平均动脉压升高。然而，这种升压反应被取消后，以剂量依赖性的方式脑室内注射的H1受体拮抗剂异丙嗪。在其他实验中，从视上核（SON），室旁核（PVN），和后下丘脑区域显微解剖的脑组织显示显着较低的总组织HA水平后60分钟的静脉内HTS输注相比，从对照动物接受等渗输注的组织。HTS输注前和输注期间PVN或SON区域的微透析显示输注期间SON中HA的细胞外浓度增加（24.4 +/- 10.9%）。HTS输注期间，PVN中细胞外HA浓度未观察到变化。这些结果支持内源性脑HA参与外周高渗性升压反应的结论。
The role of brain histamine (HA) in the pressor response to peripheral hyperosmolality was investigated in the conscious Sprague-Dawley rat. Increased mean arterial pressure was observed during a 30-min intravenous infusion of hypertonic saline (HTS; 10 microliters.100 g body wt-1 x min-1) in vehicle-treated controls (20.1 +/- 3.8 mmHg) and in animals centrally pretreated with the specific H2-antagonist, cimetidine (15.0 +/- 3.7 mmHg). However, this pressor response was abolished in a dose-dependent manner after intracerebroventricular injection of the H1 antagonist promethazine. In other experiments, brain tissue microdissected from the supraoptic nucleus (SON), paraventricular nucleus (PVN), and posterior hypothalamic region showed significantly lower levels of total tissue HA after 60 min of intravenous HTS infusion compared with tissue taken from control animals receiving an isotonic infusion. Microdialysis in the region of the PVN or SON before and during HTS infusion showed increased extracellular concentrations of HA in the SON (24.4 +/- 10.9%) during infusion. No change in extracellular HA concentration was seen in the PVN during HTS infusion. These results support the conclusion that endogenous brain HA is involved in the pressor response to peripheral hyperosmolality.