Effects of CSF ANG II and AVP on sweating in the heat-stressed patas monkey.
Effects of CSF ANG II and AVP on sweating in the heat-stressed patas monkey.
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CSF ANG II 和 AVP 对热应激帕塔猴出汗的影响。
DOI：
10.1152/jappl.1989.67.1.134
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Gisolfi,CV
中科院分区：
文献类型：
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作者：
Owen,MD;Matthes,RD;Gisolfi,CV
增加脑脊液[Na+]可降低热应激patas猴（红头猴）的出汗率（msw）。本研究确定了两种神经肽，血管紧张素II（ANG II）和精氨酸加压素（AVP），在介导这种反应的潜在作用。将含有ANG II或AVP的人工脑脊液注入暴露于41 +/- 2 ℃的伦哌隆镇静猴（n = 4）的第三脑室。以16.5微升/分钟输注溶液25分钟（总体积约413微升）。ANG II（1.25、2.5、5和10 ng/微升）倾向于降低. msw。然而，在输注过程中，只有10分钟时与1.25 ng/μ L剂量相关的下降（26%）与对照组不同（P <0.004）。该剂量在输注后20分钟使核心直肠温度升高（P <0.004）1.14 ℃。与此相反，AVP（0.5和1.5微克/微升人工脑脊液）没有显着影响.MSW相比，控制输注。在输注后20分钟，两种剂量的AVP分别使直肠温度轻微但显著地升高0.14和0.22 ℃。总之，中枢ANG II的.msw变化的幅度和时间过程表明，它不是脑脊液[Na+]升高时观察到的.msw下降的唯一介质。第三脑室AVP产生的最小效应排除了这一途径，作为AVP在脱水期间调节MSW的手段。
Increasing cerebrospinal fluid [Na+] reduces sweat rate (msw) in the heat-stressed patas monkey (Erythrocebus patas). This study determined the potential role of two neuropeptides, angiotensin II (ANG II) and arginine vasopressin (AVP), in mediating this response. Artificial cerebrospinal fluid, containing either ANG II or AVP, was infused into the third cerebral ventricle of lenperone-tranquilized monkeys (n = 4) exposed to 41 +/- 2 degrees C. Solutions were infused at 16.5 microliters/min for 25 min (total vol approximately 413 microliters). ANG II (1.25, 2.5, 5, and 10 ng/microliters) tended to decrease .msw. However, during infusion, only the decline at 10 min associated with the 1.25-ng/microliters dose (26%) was different (P less than 0.004) from control. This dose elevated (P less than 0.004) core rectal temperature by 1.14 degrees C at 20 min postinfusion. In contrast, AVP (0.5 and 1.5 micrograms/microliters artificial cerebrospinal fluid) had no significant effect on .msw compared with control infusions. Both doses of AVP produced a slight but significant increase in rectal temperature of 0.14 and 0.22 degrees C, respectively, at 20 min postinfusion. In conclusion, the magnitude and time course of the change in .msw with central ANG II suggest that it does not act as the sole mediator of the decline in .msw observed with elevated cerebrospinal fluid [Na+]. The minimal effects produced by third ventricular AVP exclude this route as a means by which AVP could modulate .msw during dehydration.