Okawara Y, Kobayashi H
Department of Biology, Faculty of Science, Toho University, Chiba, Japan.
Gen Comp Endocrinol. 1988 Jan;69(1):114-8. doi: 10.1016/0016-6480(88)90059-7.
Single intraperitoneal (ip) injections of angiotension II (ANG II) stimulated water intake for 60 min in a dose-related manner in the goldfish, Carassius auratus. Single ip injections of captopril (SQ14225), an angiotension I-converting enzyme (ACE) inhibitor, at lower doses (0.4 and 4.0 micrograms/fish), stimulated water intake for 60 min. This stimulation cannot be ascribed to an increase in levels of plasma ANG I, since ANG I (2.2 micrograms/fish) did not stimulate drinking in the presence of SQ14225 (two injections of 9.9 micrograms/fish). It is suggested that the elevated plasma ANG I concentration achieved after blockade of ACE was converted into ANG II approximately 50 min after SQ14225 injections (4.0 g/fish), when the injected SQ14225 was effectively metabolized. Thus, the newly elevated level of ANG II may have been responsible for the vigorous drinking. Higher doses of SQ14225 (40 and 200 microgram/fish) did not affect the water intake for 60 min, indicating that the rate of basal water intake is independent of the renin-angiotensin system in the goldfish.
腹腔内单次注射血管紧张素II（ANG II）能以剂量相关的方式刺激金鱼（Carassius auratus）饮水60分钟。腹腔内单次注射较低剂量（0.4和4.0微克/鱼）的卡托普利（SQ14225），一种血管紧张素I转换酶（ACE）抑制剂，也能刺激饮水60分钟。这种刺激不能归因于血浆ANG I水平的升高，因为在注射SQ14225（两次，每次9.9微克/鱼）的情况下，ANG I（2.2微克/鱼）并未刺激饮水。有人提出，在注射SQ14225（4.0微克/鱼）后约50分钟，当注射的SQ14225有效代谢时，ACE被阻断后升高的血浆ANG I浓度大约被转化为ANG II。因此，新升高的ANG II水平可能是导致剧烈饮水的原因。较高剂量的SQ14225（40和200微克/鱼）在60分钟内不影响饮水，这表明金鱼的基础饮水速率与肾素-血管紧张素系统无关。
