Purinergic mechanisms of lateral parabrachial nucleus facilitate sodium depletion-induced NaCl intake.
Purinergic receptors are present in the lateral parabrachial nucleus (LPBN), a pontine structure involved in the control of sodium intake. In the present study, we investigated the effects of α,β-methyleneadenosine 5'-triphosphate (α,β-methylene ATP, selective P2X purinergic agonist) alone or combined with pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, P2X purinergic antagonist) or suramin (non-selective P2 purinergic antagonist) injected into the LPBN on sodium depletion-induced 1.8% NaCl intake. Male Holtzman rats with stainless steel cannulas implanted into the LPBN were used. Sodium depletion was induced by treating rats with the diuretic furosemide (20mg/kg of body weight) followed by 24h of sodium-deficient diet. Bilateral injections of α,β-methylene ATP (2.0 and 4.0nmol/0.2μl) into the LPBN increased sodium depletion-induced 1.8% NaCl intake (25.3±0.8 and 26.5±0.9ml/120min, respectively, vs. saline: 15.2±1.3ml/120min). PPADS (4nmol/0.2μl) alone into the LPBN did not change 1.8% NaCl intake, however, pretreatment with PPADS into the LPBN abolished the effects of α,β-methylene ATP on 1.8% NaCl intake (16.9±0.9ml/120min). Suramin (2.0nmol/0.2μl) alone into the LPBN reduced sodium depletion-induced 1.8% NaCl intake (5.7±1.9ml/120min, vs. saline: 15.5±1.1ml/120min), without changing 2% sucrose intake or 24h water deprivation-induced water intake. The combination of suramin and α,β-methylene ATP into the LPBN produced no change of 1.8% NaCl intake (15.2±1.2ml/120min). The results suggest that purinergic P2 receptor activation in the LPBN facilitates NaCl intake, probably by restraining LPBN mechanisms that inhibit sodium intake.
Department of Physiology and Pathology, São Paulo State University, UNESP, Araraquara, SP, Brazil.
Miguel F
MF
Menezes
Silas P
SP
Barbosa
Carina A F
CA
De Andrade
José V
JV
Menani
Patrícia M
PM
De Paula
D000255:Adenosine Triphosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004326:Drinking / Q000187:drug effects; D004327:Drinking Behavior / Q000187:drug effects*; D004333:Drug Administration Routes; D005508:Food Deprivation; D008297:Male; D011149:Pons / Q000187:drug effects / Q000378:metabolism*; D058911:Purinergic P2X Receptor Agonists / Q000494:pharmacology; D058920:Purinergic P2X Receptor Antagonists / Q000494:pharmacology; D011732:Pyridoxal Phosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D051381:Rats; D058469:Receptors, Purinergic P2X; D012965:Sodium Chloride / Q000008:administration & dosage / Q000378:metabolism*; D017673:Sodium Chloride, Dietary / Q000494:pharmacology; D013395:Sucrose / Q000008:administration & dosage; D013498:Suramin / Q000494:pharmacology; D013997:Time Factors; D014868:Water Deprivation / Q000502:physiology
D058911:Purinergic P2X Receptor Agonists; D058920:Purinergic P2X Receptor Antagonists; D058469:Receptors, Purinergic P2X; D017673:Sodium Chloride, Dietary; C077792:pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid; D012965:Sodium Chloride; D013395:Sucrose; D011732:Pyridoxal Phosphate; D013498:Suramin; D000255:Adenosine Triphosphate; C002630:alpha,beta-methyleneadenosine 5'-triphosphate