ABSTRACT
Sodium chloride intake was studied in male Holtzman rats weighing 250-300 g submitted to electrolytic and chemical lesion of the cell bodies, not fibers of the amygdaloid complex. Sodium chloride (1.5 percent) intake increased in animals with electrolytic lesion of the corticomedial nucleus of the amygdala. Sodium chloride (1.5 percent) intake increased after ibotenic acid injection into the corticomedial nucleus of the amygdala to a larger extent (26.6 + or - 9.2 to 147.6 + or - 34.6 ml/5 days). The results indicate that sodium inake response can be induced by lesions, which involved only cell bodies. The fibers of passage of the corticomedial nucleus of the amygdala produce a water intake less consistent than that induced by ibotenic acid, which is more acute. The results show that cell bodies of this region of the amygdala are involved in the control of sodium chloride intake
Subject(s)
Animals , Male , Rats , Ibotenic Acid/adverse effects , Amygdala/injuries , Electrolysis/adverse effects , Rats, Sprague-Dawley , Sodium Chloride, Dietary/administration & dosageABSTRACT
We investigated the effects of ramipril, an angiotensin I-converting enzyme (ACE) inhibitor, on water intake by male Holtzman rats (250-300 g) with cannulae implanted into the lateral ventricle. Intracerebroventricular (icv) injection of ramipril (1 µg/µl) significantly reduced drinking in response to subcutaneous (sc) injection of isoprenaline (100 µg/kg) from 8.49 + or - 0.69 to 2.96 + or - 0.36 ml/2 h, polyenthyleneglycol (PEG) (30 percent w/v, 10 ml/kg) from 9.51 + or - 2.20 to 1.6 + - 0.34 ml/2 h or water deprivation for 24 h from 12.61 + or - 0.83 to 5.10 + or - 1.37 ml/2 h. Ramipril had no effect on water intake induced by cellular dehydration produced by sc injection of hypertonic saline (2 M NaCl). These results are consistent with the hypothesis that ramipril acts as an ACE-blocking agent in the brain. The possibility that ramipril is transformed to ramiprilat, the active drug, by the brain is suggested