A1 Noradrenergic Neurons Lesions Reduce Natriuresis and Hypertensive Responses to Hypernatremia in Rats

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2013-09-10
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Silva, Elaine Fernanda da
Freiria-Oliveira, Andre Henrique
Xavier Custodio, Carlos Henrique
Ghedini, Paulo Cesar
Mendes Bataus, Luiz Artur
Colombari, Eduardo
Castro, Carlos Henrique de
Colugnati, Diego Basile [UNIFESP]
Rosa, Daniel Alves
Cravo, Sergio Luiz [UNIFESP]
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Noradrenergic neurons in the caudal ventrolateral medulla (CVLM; A1 group) contribute to cardiovascular regulation. the present study assessed whether specific lesions in the A1 group altered the cardiovascular responses that were evoked by hypertonic saline (HS) infusion in non-anesthetized rats. Male Wistar rats (280-340 g) received nanoinjections of antidopamine-beta-hydroxylase-saporin (A1 lesion, 0.105 ng.nL(-1)) or free saporin (sham, 0.021 ng.nL(-1)) into their CVLMs. Two weeks later, the rats were anesthetized (2% halothane in O-2) and their femoral artery and vein were catheterized and led to exit subcutaneously between the scapulae. On the following day, the animals were submitted to HS infusion (3 M NaCl, 1.8 ml . kg(-1), b.wt., for longer than 1 min). in the sham-group (n = 8), HS induced a sustained pressor response (Delta MAP: 35 +/- 3.6 and 11 +/- 1.8 mmHg, for 10 and 90 min after HS infusion, respectively; P<0.05 vs. baseline). Ten min after HS infusion, the pressor responses of the anti-D beta H-saporin-treated rats (n = 11) were significantly smaller(Delta MAP: 18 +/- 1.4 mmHg; P<0.05 vs. baseline and vs. sham group), and at 90 min, their blood pressures reached baseline values (2 +/- 1.6 mmHg). Compared to the sham group, the natriuresis that was induced by HS was reduced in the lesioned group 60 min after the challenge (19 +/- 65.5 mM vs. 262 +/- 7.6 mM, respectively; P<0.05). in addition, A1-lesioned rats excreted only 47% of their sodium 90 min after HS infusion, while sham animals excreted 80% of their sodium. Immunohistochemical analysis confirmed a substantial destruction of the A1 cell group in the CVLM of rats that had been nanoinjected withanti-D beta H-saporin. These results suggest that medullary noradrenergic A1 neurons are involved in the excitatory neural pathway that regulates hypertensive and natriuretic responses to acute changes in the composition of body fluid.
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Plos One. San Francisco: Public Library Science, v. 8, n. 9, 11 p., 2013.
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