a2 noradrenergic lesions prevent renal sympathoinhibition induced by hypernatremia in ratsa2去甲病变预防肾sympathoinhibition老鼠体内血钠过多引起的.pdfVIP

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a2 noradrenergic lesions prevent renal sympathoinhibition induced by hypernatremia in ratsa2去甲病变预防肾sympathoinhibition老鼠体内血钠过多引起的.pdf

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a2 noradrenergic lesions prevent renal sympathoinhibition induced by hypernatremia in ratsa2去甲病变预防肾sympathoinhibition老鼠体内血钠过多引起的

A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats 1 ´ 2 ´ ˜ 2 Gustavo Rodrigues Pedrino *, Andre Henrique Freiria-Oliveira , Debora Simoes Almeida Colombari , Daniel Alves Rosa1, Sergio Luiz Cravo3 ´ ˆ ´ ˜ 1 Department of Physiological Science, Universidade Federal de Goias, Goiania, Goias, Brazil, 2 Department of Physiology and Pathology, School of Dentistry, Sao Paulo ˜ ˜ ˜ ˜ State University, Araraquara, Sao Paulo, Brazil, 3 Department of Physiology, Escola Paulista de Medicina, Universidade Federal de Sao Paulo, Sao Paulo, Sao Paulo, Brazil Abstract Renal vasodilation and sympathoinhibition are recognized responses induced by hypernatremia, but the central neural pathways underlying such responses are not yet entirely understood. Several findings suggest that A2 noradrenergic neurons, which are found in the nucleus of the solitary tract (NTS), play a role in the pathways that contribute to body fluid homeostasis and cardiovascular regulation. The purpose of this study was to determine the effects of selective lesions of A2 neurons on the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Male Wistar rats (280– 350 g) received an injection into the NTS of anti-dopamine-beta-hydroxylase-saporin (A2 lesion; 6.3 ng in 60 nl; n = 6) or free sapor