Thunhorst R L, Beltz T G, Johnson A K
Departments of Psychology and Pharmacology and the Cardiovascular Center, University of Iowa, Iowa City, Iowa 52242-1407, USA.
Am J Physiol. 1999 Jul;277(1 Pt 2):R56-65. doi: 10.1152/ajpregu.1999.277.1.r56.
We examined the role of the subfornical organ (SFO) in stimulating thirst and salt appetite using two procedures that initiate water and sodium ingestion within 1-2 h of extracellular fluid depletion. The first procedure used injections of a diuretic (furosemide, 10 mg/kg sc) and a vasodilator (minoxidil, 1-3 mg/kg ia) to produce hypotension concurrently with hypovolemia. The resulting water and sodium intakes were inhibited by intravenous administration of ANG II receptor antagonist (sarthran, 8 micrograms . kg(-1). min(-1)) or angiotensin-converting enzyme inhibitor (captopril, 2.5 mg/h). The second procedure used injections of furosemide (10 mg/kg sc) and a low dose of captopril (5 mg/kg sc) to initiate water and sodium ingestion upon formation of ANG II in the brain. Electrolytic lesions of the SFO greatly reduced the water intakes, and nearly abolished the sodium intakes, produced by these relatively acute treatments. These results contrast with earlier findings showing little effect of SFO lesions on sodium ingestion after longer-term extracellular fluid depletion.
我们采用两种在细胞外液耗竭后1 - 2小时内引发水和钠摄入的方法,研究了穹窿下器(SFO)在刺激口渴和盐食欲中的作用。第一种方法是注射利尿剂(速尿,10 mg/kg皮下注射)和血管扩张剂(米诺地尔,1 - 3 mg/kg腹腔注射),以在产生血容量减少的同时导致低血压。静脉注射ANG II受体拮抗剂(沙坦,8微克·kg⁻¹·min⁻¹)或血管紧张素转换酶抑制剂(卡托普利,2.5 mg/h)可抑制由此产生的水和钠摄入量。第二种方法是注射速尿(10 mg/kg皮下注射)和低剂量卡托普利(5 mg/kg皮下注射),以在脑内形成ANG II时引发水和钠摄入。穹窿下器的电解损伤极大地减少了这些相对急性处理所产生的水摄入量,并且几乎消除了钠摄入量。这些结果与早期的发现形成对比,早期发现表明在长期细胞外液耗竭后,穹窿下器损伤对钠摄入几乎没有影响。