Ohno N
Endocrinol Jpn. 1981 Aug;28(4):443-9. doi: 10.1507/endocrj1954.28.443.
The effects of intrahepatic portal infusion of hyperosmotic substances or angiotensin II (A II) on the plasma arginine vasopressin (pAVP) concentration were investigated. At the beginning of each experiment, rats anesthetized with sodium pentobarbital were infused with 0.9% NaCl at a rate of 0.037 ml/min via the hepatic portal vein for 30 min. Subsequent intraportal infusions of 1.4, 1.8 and 2.7% NaCl for 5 min at a rate of 0.052 ml/min raised pAVP levels from 15.6 +/- 5.2 pg/ml to 26.0 +/- 1.7, 61.5 +/- 8.8 and 37.5 +/- 6.6 pg/ml, respectively. However, subsequent intraportal infusions of 0.9 or 3.6% NaCl and intrajugular infusions of 1.8 or 3.6% NaCl did not further raise the pAVP levels. Intraportal infusions of 21 and 42% sucrose raised pAVP levels to 28.3 +/- 2.9 and 24 +/- 2.0 pg/ml, respectively, whereas glucose did not change the pAVP concentration. When A II was infused via the intraportal vessel at a rate of 30 ng/kg/min for 10, 15 or 30 min, pAVP levels became 29.3 +/- 2.7, 32.1 +/- 4.0 or 25.8 +/- 3.2 pg/kg/min respectively. PAVP levels did not change when the same dose of A II was infused into the jugular vein. The increase of pAVP induced by A II was prevented when angiotensin II analogue (A II A), 1Sar, 8Ileu-A II, was infused into portal vein simultaneously. These results not only suggest that the osmoreceptors exist in the area located somewhere within the hepatic portal vascular bed, but also that the osmoreceptors are somewhat different in nature from those of hypothalamic osmoreceptors. Furthermore, these results suggest that A II in the hepatic portal vein plays a part in controlling AVP release.
研究了肝内门静脉输注高渗物质或血管紧张素II(A II)对血浆精氨酸加压素(pAVP)浓度的影响。在每个实验开始时,用戊巴比妥钠麻醉的大鼠通过肝门静脉以0.037 ml/min的速率输注0.9% NaCl,持续30分钟。随后以0.052 ml/min的速率经门静脉输注1.4%、1.8%和2.7% NaCl 5分钟,pAVP水平分别从15.6±5.2 pg/ml升高至26.0±1.7、61.5±8.8和37.5±6.6 pg/ml。然而,随后经门静脉输注0.9%或3.6% NaCl以及经颈静脉输注1.8%或3.6% NaCl并未进一步提高pAVP水平。经门静脉输注21%和42%蔗糖分别使pAVP水平升高至28.3±2.9和24±2.0 pg/ml,而葡萄糖未改变pAVP浓度。当以30 ng/kg/min的速率经门静脉血管输注A II 10、15或30分钟时,pAVP水平分别变为29.3±2.7、32.1±4.0或25.8±3.2 pg/kg/min。当将相同剂量的A II注入颈静脉时,pAVP水平未发生变化。当同时将血管紧张素II类似物(A II A),即1Sar,8Ileu - A II注入门静脉时,A II诱导的pAVP升高被阻止。这些结果不仅表明渗透压感受器存在于肝门静脉血管床内的某个区域,而且表明这些渗透压感受器在性质上与下丘脑渗透压感受器有所不同。此外,这些结果表明肝门静脉中的A II在控制抗利尿激素释放中起作用。