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Articles in PresS, published online ahead of print May 6, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00026.2002
Submitted on January 16, 2002
Accepted on April 30, 2002
1 Catedra de Fisiologia, Universidad de Buenos Aires, Facultad de Farmacia y Bioquimica, Buenos Aires, Argentina
2 Catedra de Fisiologia, Universidad de Buenos Aires, Facultad de Farmacia y Bioquimica, Buenos Aires, Argentina; Catedra de Fisiopatologia, Universidad de Buenos Aires, Facultad de Farmacia y Bioquimica, Buenos Aires, Argentina
3 Catedra de Fisiopatologia, Universidad de Buenos Aires, Facultad de Farmacia y Bioquimica, Buenos Aires, Argentina; Catedra de Fisiologia, Universidad de Buenos Aires, Facultad de Farmacia y Bioquimica, Buenos Aires, Argentina
* To whom correspondence should be addressed. E-mail: mvatta{at}ffyb.uba.ar.
The existence of endothelin binding sites on the catecholaminergic neurons of the hypothalamus suggests that endothelins (ETs) participate in the regulation of noradrenergic transmission modulating various hypothalamic-controlled processes such as blood pressure, cardiovascular activity, etc. The effects of endothelin-1 (ET-1) and endothelin-3 (ET-3) on the neuronal release of norepinephrine (NE) as well as the receptors and intracellular pathway involved were studied in the rat anterior hypothalamus. Ten 
M ET-1 and 10 M ET-3 diminished neuronal NE release and the effect was blocked by the selective endothelin type B receptor antagonist BQ-788 (100 M). N 
-nitro-L-arginine methylester (10 µM), methylene blue (10 µM), and KT5823 (2 µM), inhibitors of nitric oxide synthase activity, guanylate cyclase and protein Kinase G respectively, prevented the inhibitory effects of both ETs on neuronal NE release. In addition, both ETs increased nitric oxide synthase activity. Further, 100 µM picrotoxin, a GABAA-receptor antagonist inhibited ET-1 and ET-3 response. Our results show that ET-1 as well as ET-3 have an inhibitory neuromodulatory effect on NE release in the anterior hypothalamus mediated by the endothelin type B receptor and the involment of a nitric oxide-dependent pathway and GABAA receptors. ET-1 and ET-3 may thus diminish available NE in the synaptic gap leading to decreased noradrenergic activity.
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