The role of brain angiotensin converting enzyme on the nocturnal thirst and sodium appetite in ovariectomized rats (683.6)

Abstract

We investigated the role of brain angiotensin converting enzyme (ACE) on nocturnal fluid intake (water and 0.3 M NaCl solution) in ovariectomized (OVX) and estradiol benzoate‐treated (EB‐OVX) rats placed in metabolic cages. We performed peripheral (100 mg/Kg) and central (50 ng/animal) captopril (CAP) administration with or without angiotensin I (ANG I; 100 ng/animal) microinjection. Both CAP administration routes reduced basal water and salt intake in OVX and EB‐OVX groups. Peripheral CAP administration inhibited fluids intake in both groups submitted to sodium depletion (sc furosemide 20 mg/Kg followed by 24 h low sodium diet) while icv CAP decreased fluids ingestion only in the EB‐OVX group. Following furocap protocol (sc furosemide 10 mg/Kg plus sc CAP 5 mg/Kg), icv CAP decreased fluids intake in both groups. Hypothalamic ACE‐1 mRNA expression was unaltered in both protocols comparing OVX vs EB‐OVX. EB replacement increased hypothalamic ACE‐2 mRNA expression in furosemide protocol, despite it has been lower in furocap than in furosemide protocol. Our results suggest that EB replacement attenuates sodium appetite in OVX rats due to the modulation of the brain ANG II activity. The increased ACE‐2 expression induced by EB replacement could be a plausible explanation taking into account other angiotensins produced in the brain may exert a counteracting ANG II signalling.Grant Funding Source: Supported by FAPERJ & CNPq