Adrenergic mechanisms of the Kölliker-Fuse/A7 area on the control of water and sodium intake.
The blockade of serotoninergic receptors with methysergide or the activation of alpha(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 alpha-adrenoceptors) alone or combined with the alpha(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 microl) 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 microl) into LPBN or KF/A7 area abolished the effects of noradrenaline (160 nmol/0.2 microl) 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 microl) 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 microg/0.2 microl) into the KF/A7 area did not alter 0.3 M NaCl or water intake. The results suggest that alpha(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.
Gasparini
S
S
Department of Physiology and Pathology, School of Dentistry, São Paulo State University-UNESP, Araraquara, SP, Brazil.
de Luca
L A
LA
Colombari
D S A
DS
de Paula
P M
PM
Barbosa
S P
SP
Menani
J V
JV
D018663:Adrenergic Agents / Q000494:pharmacology*; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D002216:Captopril / Q000494:pharmacology; D019422:Dietary Sucrose; D004327:Drinking Behavior / Q000187:drug effects* / Q000502:physiology; D005665:Furosemide / Q000494:pharmacology; D019329:Idazoxan / Q000031:analogs & derivatives / Q000494:pharmacology; D008297:Male; D045283:Natriuretic Agents / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011149:Pons / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017673:Sodium Chloride, Dietary; D014867:Water
D018663:Adrenergic Agents; D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D019422:Dietary Sucrose; D045283:Natriuretic Agents; D017673:Sodium Chloride, Dietary; D014867:Water; D005665:Furosemide; D002216:Captopril; C058525:2-methoxyidazoxan; D009638:Norepinephrine; D019329:Idazoxan