Catecholaminergic neurons in the comissural region of the nucleus of the solitary tract modulate hyperosmolality-induced responses
Catecholaminergic neurons in the comissural region of the nucleus of the solitary tract modulate hyperosmolality-induced responses
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DOI：
10.1152/ajpregu.00432.2014
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发表时间：
2015-11-01
影响因子：
2.8
通讯作者：
Colombari, Debora S. A.
中科院分区：
文献类型：
--
作者：
Freiria-Oliveira, Andre H.;Blanch, Graziela T.;Colombari, Debora S. A.
孤束核(NTS)的去甲肾上腺素A2神经元被认为对体液平衡和心血管调节有贡献。在本研究中，我们观察了损毁NTS A2神经元对2M氯化钠(2ml/只)高渗大鼠下丘脑室旁核(PVN)和视上核(SON)神经元c-Fos表达、动脉压、饮水量和尿液排泄的影响。雄性Holtzman大鼠(280-320g)在CNTs内注射抗多巴胺-β-羟基酶-皂苷(12.6 ng/60nL；CNTs/A2损毁，n=28)或免疫球蛋白G(Ig G)-皂苷(12.6 ng/60nL；假手术，n=24)。损毁CNTs/A2可增加高渗盐处理大鼠PVN内c-Fos表达的神经元数量(90+/-13个，与假手术组47+/-20个；n=4)，但不改变小细胞PVN或SON内c-Fos表达的神经元数量。与假手术组大鼠相反，2M氯化钠灌胃可使CNTS/A2损伤大鼠的动脉压升高(16+/-3，与假手术组比较：2+/-2毫米汞柱；n=9)，该作用可被加压素拮抗剂曼宁合剂(0+/-3毫米汞柱；n=10)所阻断。此外，CNTs/A2损伤增加了高渗透压诱导的水摄入量(10.5+/-1.4，与假手术组：7.7+/-0.8ml/60min；n=8-10)，但不改变肾脏对高渗透压的反应。结果表明，依赖于CNTs/A2神经元的抑制机制减少了水的摄入量，并减少了对血浆渗透压急剧增加的加压素依赖的升压反应。
Noradrenergic A2 neurons of the nucleus of the solitary tract (NTS) have been suggested to contribute to body fluid homeostasis and cardiovascular regulation. In the present study, we investigated the effects of lesions of A2 neurons of the commissural NTS (cNTS) on the c-Fos expression in neurons of the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, arterial pressure, water intake, and urinary excretion in rats with plasma hyperosmolality produced by intragastric 2 M NaCl (2 ml/rat). Male Holtzman rats (280-320 g) received an injection of anti-dopamine-beta-hydroxylase-saporin (12.6 ng/60 nl; cNTS/A2-lesion, n = 28) or immunoglobulin G (IgG)-saporin (12.6 ng/60 nl; sham, n = 24) into the cNTS. The cNTS/A2 lesions increased the number of neurons expressing c-Fos in the magnocellular PVN in rats treated with hypertonic NaCl (90 +/- 13, vs. sham: 47 +/- 20; n = 4), without changing the number of neurons expressing c-Fos in the parvocellular PVN or in the SON. Contrary to sham rats, intragastric 2 M NaCl also increased arterial pressure in cNTS/A2-lesioned rats (16 +/- 3, vs. sham: 2 +/- 2 mmHg 60 min after the intragastric load; n = 9), an effect blocked by the pretreatment with the vasopressin antagonist Manning compound (0 +/- 3 mmHg; n = 10). In addition, cNTS/A2 lesions enhanced hyperosmolality-induced water intake (10.5 +/- 1.4, vs. sham: 7.7 +/- 0.8 ml/60 min; n = 8-10), without changing renal responses to hyperosmolality. The results suggest that inhibitory mechanisms dependent on cNTS/A2 neurons reduce water intake and vasopressin-dependent pressor response to an acute increase in plasma osmolality.