Thunhorst R L, Fitts D A, Simpson J B
Am J Physiol. 1987 Feb;252(2 Pt 2):R409-18. doi: 10.1152/ajpregu.1987.252.2.R409.
Several experiments tested whether the subfornical organ (SFO) is necessary for water or NaCl intake arising from angiotensin-converting enzyme (CE) blockade with captopril (CAP) in the drinking fluids (0.1 mg/ml). Peripheral CAP was given to rats acutely following 24-h water deprivation or chronically over several days, either with water alone available for drinking or with 0.3 M NaCl in choice with water. Control rats drank more water, and NaCl when it was available, during CAP treatment, whereas rats with SFO damage increased NaCl intake only. CAP decreased urinary volume (UV) and increased urinary potassium excretion (UKV) during rehydration with only water available and increased urinary sodium excretion (UNaV) with NaCl present. Regardless of CAP treatment, rats with SFO damage had increased electrolyte concentrations and excretions during rehydration with only water available and increased UK with NaCl present, compared with controls. Oral CAP did not have an aversive taste at the dose used here. We conclude that the SFO is necessary for CAP-enhanced water, but not NaCl, intake and suggest that different neurological mechanisms control ingestion of each fluid during CAP.
进行了多项实验，以测试穹窿下器（SFO）对于饮用含卡托普利（CAP）（0.1毫克/毫升）的饮液时因血管紧张素转换酶（CE）阻断而引发的水或氯化钠摄入是否必要。在24小时禁水后，对大鼠急性给予外周CAP，或在数天内慢性给药，大鼠可单独饮水，也可在水和0.3 M氯化钠之间进行选择饮用。对照大鼠在CAP治疗期间饮用更多的水，有氯化钠时也会饮用氯化钠，而穹窿下器受损的大鼠仅增加了氯化钠的摄入量。在仅提供水进行补液期间，CAP减少了尿量（UV）并增加了尿钾排泄量（UKV），有氯化钠存在时则增加了尿钠排泄量（UNaV）。与对照相比，无论CAP治疗如何，穹窿下器受损的大鼠在仅提供水进行补液期间电解质浓度和排泄量增加，有氯化钠存在时尿钾增加。此处使用的口服CAP剂量没有厌恶味道。我们得出结论，穹窿下器对于CAP增强的水摄入是必要的，但对于氯化钠摄入不是必要的，并表明在CAP期间，不同的神经机制控制每种液体的摄取。
