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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Department of Physiology, Tohoku University School of Dentistry, Sendai, Japan.

Gen Pharmacol. 1991;22(5):825-9. doi: 10.1016/0306-3623(91)90214-q.

Subcutaneous (s.c.) administration of compound 48/80 elicited the increases of water intake, plasma beta-endorphin-like immunoreactivity, hypothalamic 3-methoxy-4-hydroxyphenylethyleneglycol sulfate and Hct in the rats. 2. The s.c. pretreatment of naloxone reduced the compound 48/80-induced water intake but had no effects on other variables. 3. Intracerebroventricular (i.c.v.) injection of naloxone attenuated the compound 48/80- and i.c.v. injected angiotensin II (ANG II)-induced water intake. 4. The hypothalamic norepinephrine metabolism was increased by s.c. injection of compound 48/80 but not by i.c.v. ANG II. 5. The present data suggest the possible involvement of opioid peptide (beta-endorphin) on the compound 48/80- and ANG II-induced thirst. However, it is uncertain whether hypothalamic norepinephrine is involved in the hypovolemic thirst mediated via stimulation of renin-angiotensin system.

给大鼠皮下注射化合物48/80会引起其饮水量增加、血浆β-内啡肽样免疫反应性升高、下丘脑3-甲氧基-4-羟基苯乙二醇硫酸盐含量增加以及血细胞比容升高。2. 皮下注射纳洛酮进行预处理可减少化合物48/80诱导的饮水量，但对其他变量无影响。3. 脑室内注射纳洛酮可减弱化合物48/80和脑室内注射血管紧张素II（ANG II）诱导的饮水量。4. 皮下注射化合物48/80可增加下丘脑去甲肾上腺素代谢，但脑室内注射ANG II则不会。5. 目前的数据表明阿片肽（β-内啡肽）可能参与了化合物48/80和ANG II诱导的口渴。然而，下丘脑去甲肾上腺素是否参与通过刺激肾素-血管紧张素系统介导的低血容量性口渴尚不确定。

Department of Physiology, Tohoku University School of Dentistry, Sendai, Japan.

Gen Pharmacol. 1991;22(5):825-9. doi: 10.1016/0306-3623(91)90214-q.

Subcutaneous (s.c.) administration of compound 48/80 elicited the increases of water intake, plasma beta-endorphin-like immunoreactivity, hypothalamic 3-methoxy-4-hydroxyphenylethyleneglycol sulfate and Hct in the rats. 2. The s.c. pretreatment of naloxone reduced the compound 48/80-induced water intake but had no effects on other variables. 3. Intracerebroventricular (i.c.v.) injection of naloxone attenuated the compound 48/80- and i.c.v. injected angiotensin II (ANG II)-induced water intake. 4. The hypothalamic norepinephrine metabolism was increased by s.c. injection of compound 48/80 but not by i.c.v. ANG II. 5. The present data suggest the possible involvement of opioid peptide (beta-endorphin) on the compound 48/80- and ANG II-induced thirst. However, it is uncertain whether hypothalamic norepinephrine is involved in the hypovolemic thirst mediated via stimulation of renin-angiotensin system.

给大鼠皮下注射化合物48/80会引起其饮水量增加、血浆β-内啡肽样免疫反应性升高、下丘脑3-甲氧基-4-羟基苯乙二醇硫酸盐含量增加以及血细胞比容升高。2. 皮下注射纳洛酮进行预处理可减少化合物48/80诱导的饮水量，但对其他变量无影响。3. 脑室内注射纳洛酮可减弱化合物48/80和脑室内注射血管紧张素II（ANG II）诱导的饮水量。4. 皮下注射化合物48/80可增加下丘脑去甲肾上腺素代谢，但脑室内注射ANG II则不会。5. 目前的数据表明阿片肽（β-内啡肽）可能参与了化合物48/80和ANG II诱导的口渴。然而，下丘脑去甲肾上腺素是否参与通过刺激肾素-血管紧张素系统介导的低血容量性口渴尚不确定。