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血管加压素介导去卵巢恒河猴低血糖诱导的促黄体生成素分泌抑制。

Vasopressin mediates hypoglycemia-induced inhibition of luteinizing hormone secretion in the ovariectomized rhesus monkey.

作者信息

Heisler L E, Tumber A J, Reid R L, van Vugt D A

机构信息

Department of Physiology, Queen's University, Kingston, Canada.

出版信息

Neuroendocrinology. 1994 Sep;60(3):297-304. doi: 10.1159/000126762.

Abstract

The objective of the present study was to examine the role of vasopressin in the regulation of LH secretion in the rhesus monkey. The effect of vasopressin administration on basal LH secretion and vasopressin antagonism on stress-induced inhibition of LH secretion were examined. Intracerebroventricular (i.c.v.) infusion of vasopressin (20 micrograms/h) to chair restrained ovariectomized rhesus monkeys (n = 5) decreased the area under the LH curve by -51.61 +/- 13.73 ng/ml/h compared to -8.35 +/- 7.11 ng/ml/h following infusion of artificial CSF (aCSF; p = 0.021). This effect was independent of any change in mean arterial pressure. Subsequently, the role of vasopressin in hypoglycemia-induced suppression of LH was examined. Administration of insulin (1 U/kg BW) to chair-restrained ovariectomized rhesus monkeys decreased the area under the LH curve by -60.88 +/- 19.77 ng/ml/h. The decrease in LH was significantly different from that observed in aCSF-infused euglycemic controls which exhibited a slight decrease in LH (-8.35 +/- 7.11 ng/ml/h; p = 0.036). In contrast, the area under the LH curve was increased slightly (1.42 +/- 11.93 ng/ml/h) when insulin administration was combined with i.c.v. infusion of the vasopressin antagonist [deaminopenicillamine1, O-methyl-tyrosine2, arginine8]-vasopressin (120 micrograms/h; p = 0.013 vs. insulin only). The demonstration that vasopressin administration inhibits LH secretion whereas vasopressin antagonism prevents hypoglycemia-induced LH suppression suggests that vasopressin is a physiological inhibitor of LH secretion in the rhesus monkey.

摘要

本研究的目的是检验血管加压素在恒河猴促黄体生成素(LH)分泌调节中的作用。研究了给予血管加压素对基础LH分泌的影响以及血管加压素拮抗剂对应激诱导的LH分泌抑制的作用。对坐在椅子上受限制的去卵巢恒河猴(n = 5)进行脑室内(i.c.v.)输注血管加压素(20微克/小时),与输注人工脑脊液(aCSF)后相比,LH曲线下面积减少了-51.61±13.73纳克/毫升/小时,而输注aCSF后为-8.35±7.11纳克/毫升/小时(p = 0.021)。这种作用与平均动脉压的任何变化无关。随后,研究了血管加压素在低血糖诱导的LH抑制中的作用。对坐在椅子上受限制的去卵巢恒河猴给予胰岛素(1单位/千克体重),使LH曲线下面积减少了-60.88±19.77纳克/毫升/小时。LH的减少与输注aCSF的血糖正常对照组中观察到的情况有显著差异,后者的LH略有下降(-8.35±7.11纳克/毫升/小时;p = 0.036)。相反,当胰岛素给药与i.c.v.输注血管加压素拮抗剂[脱氨青霉胺1,O-甲基酪氨酸2,精氨酸8]-血管加压素(120微克/小时)联合使用时,LH曲线下面积略有增加(1.42±11.93纳克/毫升/小时;与仅用胰岛素相比,p = 0.013)。给予血管加压素可抑制LH分泌,而血管加压素拮抗剂可防止低血糖诱导的LH抑制,这一证明表明血管加压素是恒河猴LH分泌的生理抑制剂。

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