Saad W A, de Arruda Camargo L A, Morita N, Antunes-Rodrigues J, Covian M R
Acta Physiol Lat Am. 1979;29(6):323-32.
Rats bearing lesions in the septal area (SA), or in the subfornical organ (SFO) or simultaneously in both regions were submitted to various thirst-eliciting procedures. The rats with hyperdipsia induced by lesion of the SA drank more water than either normal rats or SFO-lesioned animals under the same thirst-eliciting or angiotensin-liberating stimuli (polyethyleneglycol, isoproterenol, water deprivation and ligation of the inferior vena cava). The overdrinking elicited by SA lesions was blocked after SFO lesions. Neither hypovolemia, nor hypotension or water deprivation could elicit increased water intake in SFO-lesioned animals even after destruction of the SA. Animals with SFO lesions did not show increase of the water intake after cellular dehydration. The results obtained suggest that the SFO acts as the main structure in the regulation of water intake elicited by angiotensin with two opposite effects: one direct, facilitating water intake and the other indirect inhibiting the SA. The SA has an inhibitory effect on the SFO and on water intake.
对在隔区（SA）、穹窿下器（SFO）或同时在这两个区域有损伤的大鼠进行了各种引发口渴的实验。在相同的引发口渴或释放血管紧张素的刺激（聚乙二醇、异丙肾上腺素、禁水和结扎下腔静脉）下，由SA损伤诱导产生烦渴的大鼠比正常大鼠或SFO损伤的动物饮水更多。SFO损伤后，SA损伤引发的过度饮水被阻断。即使在破坏SA后，血容量减少、低血压或禁水都不能使SFO损伤的动物饮水增加。SFO损伤的动物在细胞脱水后未表现出饮水量增加。所得结果表明，SFO作为调节血管紧张素引发的饮水的主要结构，具有两种相反的作用：一种是直接促进饮水，另一种是间接抑制SA。SA对SFO和饮水具有抑制作用。
