Central oxytocin systems may mediate a cardiovascular response to acute stress in rats.
Central oxytocin systems may mediate a cardiovascular response to acute stress in rats.
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中枢催产素系统可能介导大鼠对急性应激的心血管反应。
DOI：
10.1152/ajpheart.1989.256.5.h1369
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Gruber,KA
中科院分区：
文献类型：
--
作者：
Callahan,MF;Kirby,RF;Cunningham,JT;Eskridge-Sloop,SL;Johnson,AK;McCarty,R;Gruber,KA
用三种实验模型研究了中枢神经系统精氨酸加压素(AVP)和催产素(Oxy)在急性应激心血管反应中的作用：中枢AVP-Oxy受体的药理拮抗作用；室旁核(PVN)的损毁；遗传缺乏AVP合成的大鼠，即Brattleboro系。中枢应用AVP-Oxy拮抗剂可消除急性足部电击应激后心率(HR)的增加。中枢给药组心率增加15+/-17(SE)次/分，静脉给药组增加66+/-17次/分，脑室注射拮抗剂组增加101+/-14次/分。在第二项研究中，PVN的电解损伤也阻止了应激后出现的心率增加，PVN损伤大鼠为20+/-12次/分钟，假损伤大鼠为74+/-25次/分钟，而损伤未破坏PVN的大鼠为93+/-7次/分钟。在最后一项研究中，Brattleboro大鼠的反应相当于它们的Long-Evans对照组(分别为131+/-13和147+/-12次/分钟)，即后叶加压素合成基因缺陷的大鼠。在每一项研究中，控制组和试验组的血压对应激源的反应是相同的。这些研究结果表明，起源于或穿过下丘脑室旁核的神经肽系统可能在心血管应激反应中发挥重要作用，并进一步提示中枢氧合系统可能是介导这一反应的途径之一。
The role of central nervous system arginine vasopressin (AVP) and oxytocin (OXY) in the cardiovascular response to acute stress was examined using three experimental models: pharmacological antagonism of central AVP-OXY receptors; lesions of the paraventricular nucleus (PVN); and rats genetically lacking in AVP synthesis, i.e., the Brattleboro strain. Central administration of an AVP-OXY antagonist abolished the increase in heart rate (HR) seen following acute footshock stress. The group receiving centrally administered antagonist increased HR 15 +/- 17 (SE) beats/min, whereas, in contrast, the group receiving intravenous administration of the antagonist showed a 66 +/- 17 beats/min increase, and the group receiving intraventricular antagonist vehicle showed a 101 +/- 14 beats/min increase in response to stress. In a second study, electrolytic lesions of the PVN also blocked the increase in HR seen following stress, 20 +/- 12 beats/min for PVN-lesioned rats, 74 +/- 25 beats/min for sham lesion rats, and 93 +/- 7 beats/min for rats with a lesion not destroying the PVN. In the final study, the responses of Brattleboro rats, i.e., rats genetically deficient in vasopressin synthesis, were equivalent to their Long-Evans controls (131 +/- 13 and 147 +/- 12 beats/min, respectively). In each of these studies, the blood pressure responses to the stressor were equivalent for control and experimental groups. The results of these studies suggest that a neuropeptide system originating in or passing through the PVN may play an important role in the cardiovascular responses to stress and further suggest that the central OXY system may be one pathway mediating this response.