Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás,Goiânia, Goiás, Brazil.
PLoS One. 2013 Sep 10;8(9):e73187. doi: 10.1371/journal.pone.0073187. eCollection 2013.
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-β-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 O2) 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 (ΔMAP: 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-DβH-saporin-treated rats (n = 11)were significantly smaller(ΔMAP: 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 (196±5.5 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-DβH-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.
尾侧腹外侧髓质（CVLM；A1 群）中的去甲肾上腺素能神经元有助于心血管调节。本研究评估了 A1 群中的特定损伤是否改变了非麻醉大鼠高渗盐水（HS）输注引起的心血管反应。雄性 Wistar 大鼠（280-340g）接受 CVLM 中的抗多巴胺-β-羟化酶-相思豆毒素（A1 损伤，0.105ng.nL（-1））或游离相思豆毒素（假手术，0.021ng.nL（-1））的纳米注射。两周后，大鼠被麻醉（2%氟烷中的 O2），并将其股动脉和静脉插管，皮下引出至肩胛骨之间。次日，动物接受 HS 输注（3MNaCl，1.8ml•kg（-1），体重，持续 1 分钟以上）。在假手术组（n=8）中，HS 引起持续的升压反应（ΔMAP：分别在 HS 输注后 10 和 90 分钟为 35±3.6 和 11±1.8mmHg；P<0.05 与基线相比）。HS 输注后 10 分钟，抗 DβH-相思豆毒素处理大鼠的升压反应明显较小（ΔMAP：18±1.4mmHg；P<0.05 与基线和假手术组相比），90 分钟时，它们的血压达到基线值（2±1.6mmHg）。与假手术组相比，损伤组在挑战后 60 分钟时 HS 诱导的利钠作用降低（分别为 196±5.5mM 和 262±7.6mM；P<0.05）。此外，HS 输注后 90 分钟，A1 损伤大鼠仅排泄其钠的 47%，而假手术动物排泄其钠的 80%。免疫组织化学分析证实，接受抗 DβH-相思豆毒素纳米注射的大鼠 CVLM 中的 A1 细胞群受到了实质性破坏。这些结果表明，延髓去甲肾上腺素能 A1 神经元参与调节体液组成急性变化的高血压和利钠反应的兴奋性神经通路。
