Interaction between brain L-type calcium channels and alpha(2)-adrenoceptors in the inhibition of sodium appetite
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Data
2002-03-22
Autores
De Luca, L. A.
Sugawara, A. M.
Pereira, DTB
David, R. B.
Menani, José Vanderlei [UNESP]
Título da Revista
ISSN da Revista
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Editor
Elsevier B.V.
Resumo
Calcium channels mediate the actions of many drugs. The present work investigated whether diltiazem, an L-type calcium channel blocker, alters the inhibition of sodium appetite induced by noradrenaline and the alpha(2)-adrenoceptor agonist clonidine. Adult male Holtzman rats (N=4-8) with cannula implanted into the third cerebral ventricle were submitted to sodium depletion {furosemide sc+24-h removal of ambiente sodium). Sodium depleted control animals that received 0.9% NaCl as vehicle injected intracerebroventricularly (i.c.v) ingested 13.0+/-1.5 ml/120 min of 1.8% NaCl. Intracerebroventricular injection of either noradrenaline (80 nmol) or clonidine (20 nmol) inhibited 1.8% NaCl intake from 70 to 90%. Prior i.c.v. injection of diltiazem (6-48 nmol) inhibited from 50 to 100% the effect of noradrenaline and clonidine in a dose-response manner. Diltiazem alone at 100 nmol inhibited, but at 50 nmol had no effect on, sodium appetite. The results suggest: (1) common ionic mechanisms involving calcium channels for the inhibition that noradrenaline and clonidine exert on sodium appetite and (2) a dual role for the benzothiazepine site of L-type calcium channels in the control of sodium appetite. (C) 2002 Elsevier B.V. B V. All rights reserved.
Descrição
Palavras-chave
diltiazem, clonidine, noradrenaline, dehydration, sodium depletion, salt intake
Como citar
Brain Research. Amsterdam: Elsevier B.V., v. 931, n. 1, p. 1-4, 2002.