期刊论文详细信息
PHYSIOLOGY & BEHAVIOR 卷:106
Central kappa opioid receptors modulate salt appetite in rats
Article
Nascimento, A. I. R.1,3  Ferreira, H. S.2  Saraiva, R. M.3  Almeida, T. S.3  Fregoneze, J. B.3 
[1] Univ Estadual Sudoeste Bahia, Dept Biol Sci, BR-45200000 Jequie, BA, Brazil
[2] Bahia State Univ, Dept Life Sci, BR-41195001 Salvador, BA, Brazil
[3] Univ Fed Bahia, Hlth Sci Inst, Dept Physiol, BR-40110100 Salvador, BA, Brazil
关键词: Kappa opioid receptors;    Salt intake;    Sodium depletion;    Angiotensin;   
DOI  :  10.1016/j.physbeh.2012.03.028
来源: Elsevier
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【 摘 要 】

The role of the central opioid system in the control of water and salt intake is complex, with both stimulatory and inhibitory effects having been observed. The aim of the present study was to investigate the participation of the central kappa-opioid receptors in the control of salt appetite. Male Wistar rats were submitted to two different experimental protocols: sodium deficit produced by the diuretic, furosemide, and brain angiotensinergic stimulation in rats under normal sodium balance. Lateral ventricle (LV) injections of Nor-binaltorphimine (Nor-BNI) at different doses (5, 10 and 20 nmol) inhibited hypertonic saline solution (1.5%) intake in sodium-depleted rats. The salt appetite induced by an LV injection of angiotensin II (AngII) (10 ng) was also blocked by Nor-BNI injections into the LV, while no significant change was observed in water intake. Furthermore, the decrease in salt intake seems not to have been due to a general inhibition of locomotor activity or to any change in palatability, since central administration of Nor-BNI failed to modify the intake of a 0.1% saccharin solution when the animals were submitted to a dessert test or to induce any significant locomotor deficit in the open-field test. Also the central administration of Nor-BNI was unable to modify blood pressure in sodium-depleted animals. The present results suggest that activation of endogenous kappa-opioid receptors modulates salt appetite induced by sodium depletion and by central angiotensinergic stimulation in rats. (C) 2012 Elsevier Inc. All rights reserved.

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