Schmid H A, Schäfer F, Simon E
Max-Planck-Institut für Physiologische und Klinische Forschung, W.G. Kerckhoff-Institut, Bad Nauheim, Germany.
Neurosci Lett. 1995 Mar 10;187(3):149-52. doi: 10.1016/0304-3940(95)11360-9.
Angiotensin II (ANGII) is known to activate neurons in the subfornical organ (SFO) of mammals and birds and this activation is regarded as the basis for the ANGII induced increase in water intake. Application of the nitric oxide (NO) donor sodium nitroprusside inhibited the activity in 10 out of 12 duck SFO neurons, 8 of which were in addition excited by ANGII. These data, in combination with the histochemical detection of NO synthase in the duck SFO, demonstrate the involvement of NO in SFO mediated responses and might represent the cellular basis for the observed opposite effects of ANGII and NO on water intake.
已知血管紧张素II(ANGII)可激活哺乳动物和鸟类穹窿下器(SFO)中的神经元,这种激活被认为是ANGII诱导饮水量增加的基础。一氧化氮(NO)供体硝普钠的应用抑制了12只鸭SFO神经元中10只的活性,其中8只还受到ANGII的兴奋。这些数据,结合在鸭SFO中对NO合酶的组织化学检测,证明了NO参与SFO介导的反应,并且可能代表了观察到的ANGII和NO对饮水量产生相反作用的细胞基础。