el Ghissassi M, Thornton S N, Nicolaïdis S
Laboratoire de Neurobiologie des Régulations, Centre National de la Recherche Scientifique, Collège de France, Paris.
Am J Physiol. 1995 Jun;268(6 Pt 2):R1401-5. doi: 10.1152/ajpregu.1995.268.6.R1401.
The angiotensin receptor specificity, with respect to fluid intake, of the organum cavum prelamina terminalis (OCPLT), a recently discovered discrete forebrain structure with high sensitivity to angiotensin II (ANG II), was investigated. ANG II (10 ng) microinjected into the OCPLT significantly increased water consumption but did not induce intake of a hypertonic (3%) NaCl solution. Losartan, an ANG II type 1 (AT1) receptor-specific antagonist, produced dose-related (1-100 ng) inhibition of ANG II-induced drinking. The ANG II type 2 receptor-specific antagonist CGP-42112A was ineffective. Intake of the 3% NaCl solution in response to microinjection of either of the antagonists into the OCPLT was never observed. These findings suggest that water intake produced by microinjection of ANG II into the OCPLT is mediated by AT1 receptors uniquely and that, in contrast to other regions of the brain, these receptors do not induce salt intake when stimulated by ANG II.
终板前腔器官（OCPLT）是最近发现的对血管紧张素II（ANG II）高度敏感的离散前脑结构，研究了其在液体摄入方面的血管紧张素受体特异性。向OCPLT微量注射10 ng的ANG II可显著增加水的消耗量，但不会引起高渗（3%）NaCl溶液的摄入。氯沙坦是一种血管紧张素II 1型（AT1）受体特异性拮抗剂，可产生与剂量相关（1-100 ng）的对ANG II诱导饮水的抑制作用。血管紧张素II 2型受体特异性拮抗剂CGP-42112A无效。向OCPLT微量注射任何一种拮抗剂均未观察到对3% NaCl溶液的摄入。这些发现表明，向OCPLT微量注射ANG II所产生的水摄入是由AT1受体独特介导的，并且与大脑的其他区域不同，这些受体在受到ANG II刺激时不会诱导盐摄入。
