Adrenergic mechanisms of the Kölliker-Fuse/A7 area on the control of water and sodium intake

Abstract

The blockade of serotoninergic receptors with methysergide or the activation of α 2-adrenoceptors with moxonidine into the lateral parabrachial nucleus (LPBN) increases water and 0.3 M NaCl intake in rats treated with furosemide (FURO) combined with captopril (CAP). In the present study we investigated the effects of bilateral injections of noradrenaline (the endogenous neurotransmitter for α-adrenoceptors) alone or combined with the α 2-adrenoceptor antagonist RX 821002 into the LPBN or into the rostral portion of the Kölliker-Fuse nucleus that includes also the A7 area (KF/A7 area) on FURO+CAP-induced water and 0.3 M NaCl intake. Male Holtzman rats with bilateral stainless steel guide-cannulas implanted into KF/A7 area or LPBN were used. FURO+CAP-induced 0.3 M NaCl intake strongly increased after bilateral injections of noradrenaline (80 or 160 nmol/0.2 μl) into LPBN (26.5±5.9 and 20.7±2.0 ml/2 h versus saline: 4.4±0.9 ml/2 h) or into the KF/A7 area (31.5±6.1 and 25.9±4.7 ml/2 h versus saline: 7.2±1.6 ml/2 h). Water intake increased with noradrenaline injected in KF/A7 area, however, this treatment reduced 0.06 M sucrose intake, suggesting that the increase of water and NaCl intake is not related to non-specific effect. Bilateral injections of RX 821002 (160 nmol/0.2 μl) into LPBN or KF/A7 area abolished the effects of noradrenaline (160 nmol/0.2 μl) in the same areas on 0.3 M NaCl intake (7.5±2.5 and 9.8±4.4 ml/2 h, respectively). Moxonidine (0.5 nmol/0.2 μl) injected bilaterally into the KF/A7 area increased 0.3 M NaCl intake (39.5±6.3 ml/3 h) and water intake, while methysergide (4 μg/0.2 μl) into the KF/A7 area did not alter 0.3 M NaCl or water intake. The results suggest that α 2-adrenoceptor activation is a common mechanism in the KF/A7 area and LPBN to facilitate sodium intake. However, the serotonergic mechanism is present in LPBN, not in the KF/A7 area.