Blood pressure increases after injection of neuropeptide Y into posterior hypothalamic nucleus.
Blood pressure increases after injection of neuropeptide Y into posterior hypothalamic nucleus.
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下丘脑后核注射神经肽Y后血压升高。
DOI：
10.1152/ajpheart.1988.254.5.h879
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Westfall,TC
中科院分区：
文献类型：
--
作者：
Martin,JR;Beinfeld,MC;Westfall,TC
将神经肽Y（NPY；0.235-2.35 nmol）单侧显微注射到下丘脑后核中，发现乌拉坦麻醉的大鼠的平均动脉压（MAP）出现浓度依赖性增加。单侧给予下丘脑后核组胺（0.543-17.9 nmol）也可引发浓度依赖性升压反应。在给予 5.43 nmol 组胺前 10 分钟，将 30 nmol 组胺 H1 受体拮抗剂氯苯那敏（而不是 43.5 nmol 组胺 H2 受体拮抗剂西咪替丁）注入下丘脑后核，显着减弱组胺诱导的升压反应。这些浓度的扑尔敏或西咪替丁不会影响 MAP 的增加，而 MAP 的增加可能是通过将 5.48 nmol 胆碱能毒蕈碱激动剂卡巴胆碱注射到下丘脑后核中引起的。然而，在给予卡巴胆碱之前10分钟，将12 nmol胆碱能毒蕈碱拮抗剂阿托品注射到下丘脑后核中，可以完全阻断卡巴胆碱诱导的MAP增加。该阿托品浓度不影响组胺诱导的升压反应。在 2.35 nmol NPY 前 10 分钟，将阿托品或扑尔敏注射到下丘脑后核，可显着减弱 NPY 引起的升压反应。另一方面，西咪替丁不能显着影响 NPY 引起的 MAP 增加。这些结果表明，给予下丘脑后核的 NPY 可以引发升压反应，并且这种升压反应可能涉及局部组胺能和胆碱能神经元通路。
Unilateral microinjection of neuropeptide Y (NPY; 0.235-2.35 nmol) into the posterior hypothalamic nucleus was found to evoke a concentration-dependent increase in mean arterial pressure (MAP) of Urethane-anesthetized rats. Concentration-dependent pressor responses were also elicited by unilateral administration of histamine (0.543-17.9 nmol) into the posterior hypothalamic nucleus. Administration of 30 nmol of the histamine H1-receptor antagonist, chlorpheniramine, but not 43.5 nmol of the histamine H2-receptor antagonist, cimetidine, into the posterior hypothalamic nucleus 10 min before 5.43 nmol histamine administration, significantly attenuated the histamine-induced pressor response. These concentrations of chlorpheniramine or cimetidine did not affect the increase in MAP, which could be evoked by the administration of 5.48 nmol of the cholinergic muscarinic agonist carbachol into the posterior hypothalamic nucleus. The carbachol-induced increase in MAP was, however, completely blocked by administration of 12 nmol of the cholinergic muscarinic antagonist atropine into the posterior hypothalamic nucleus 10 min before carbachol administration. This concentration of atropine did not affect the histamine-induced pressor response. Administration of atropine or chlorpheniramine into the posterior hypothalamic nucleus 10 min before 2.35 nmol NPY significantly attenuated the pressor response evoked by NPY. Cimetidine, on the other hand, was unable to significantly affect the increase in MAP evoked by NPY. These results demonstrate that NPY administered into the posterior hypothalamic nucleus can elicit a pressor response, and that this pressor response might involve local histaminergic and cholinergic neuronal pathways.