Nermo-Lindquist E, Kadekaro M, Terrell M L, Nassar J, Lekan H, Freeman S
Division of Neurosurgery, University of Texas Medical Branch, Galveston 77550.
Peptides. 1990 Jul-Aug;11(4):837-42. doi: 10.1016/0196-9781(90)90201-f.
Previous studies have shown that angiotensin II (ANG II) increases glucose utilization in the subfornical organ and stimulates drinking behavior. We investigated with the deoxyglucose method whether atriopeptin III, an atrial natriuretic peptide (ANP), would prevent this enhanced glucose metabolism and interfere with the drinking response in the presence of ANG II. Two rat models with high circulating levels of ANG II were studied: the homozygous Brattleboro and ANG II-infused Sprague-Dawley rats. ANP decreased the normally enhanced glucose utilization in the subfornical organ in the Brattleboro rat and inhibited ANG II-stimulated glucose metabolism in the subfornical organ of Sprague-Dawley rats. This effect was accompanied by decreased ANG II-stimulated water intake. These findings indicate that ANP may act at the level of subfornical organ to antagonize the dipsogenic action of ANG II.
先前的研究表明，血管紧张素II（ANG II）可增加穹窿下器中的葡萄糖利用并刺激饮水行为。我们用脱氧葡萄糖法研究了心房利钠肽（ANP）中的心房肽III是否会在存在ANG II的情况下阻止这种增强的葡萄糖代谢并干扰饮水反应。研究了两种ANG II循环水平较高的大鼠模型：纯合布拉特洛维大鼠和注入ANG II的斯普拉格-道利大鼠。心房肽III降低了布拉特洛维大鼠穹窿下器中正常增强的葡萄糖利用，并抑制了斯普拉格-道利大鼠穹窿下器中ANG II刺激的葡萄糖代谢。这种作用伴随着ANG II刺激的水摄入量减少。这些发现表明，心房肽III可能在穹窿下器水平发挥作用，以拮抗ANG II的致渴作用。
