Kuchel O, Debinski W, Buu N T, Cantin M, Genest J
Laboratory of the Autonomic Nervous System, Clinical Research Institute of Montreal, Hôtel-Dieu de Montréal Hospital, Quebec, Canada.
Hypertension. 1988 Feb;11(2 Pt 2):I47-51. doi: 10.1161/01.hyp.11.2_pt_2.i47.
Because previous data have suggested a dependence of ganglionic atrial natriuretic factor (ANF) content on preganglionic cholinergic input, we investigated the possibility that the increased neural activity observed in spontaneously hypertensive rats (SHR) may be reflected by ganglionic immunoreactive ANF levels. Four-week-old normotensive SHR had celiac ganglionic immunoreactive ANF values comparable to those of Wistar-Kyoto rats (WKY). When they became hypertensive, however, at 12 weeks of age, the SHR manifested higher immunoreactive ANF levels in celiac ganglia than the WKY group (25.3 +/- 2.6 vs 14.5 +/- 1.7 pg/ganglion; p less than 0.01), but there were no differences in levels in the superior cervical and nodose ganglia. The values in celiac ganglia were quadrupled on the average in hypertensive Dahl salt-sensitive rats under the influence of an 8% salt intake for 5 weeks, but no difference was noted in any of these ganglia between this group and their salt-resistant partners. The celiac and superior cervical ganglionic immunoreactive ANF content in normotensive Sprague-Dawley rats was higher with high salt than with normal salt intake. Hypertensive rats treated with deoxycorticosterone acetate (DOCA)-salt and sham-treated controls showed immunoreactive ANF concentrations in celiac ganglia similar to those detected in Dahl rats but, again, no differences were found between groups. Thus, hypertensive SHR, compared to WKY, have higher celiac ganglionic immunoreactive ANF levels, unlike Dahl salt-sensitive and DOCA-salt animals relative to their respective controls. This increase is unique to SHR (although all three models have elevated plasma immunoreactive ANF when they are hypertensive) and to the celiac ganglia.(ABSTRACT TRUNCATED AT 250 WORDS)
由于先前的数据表明神经节心房利钠因子（ANF）含量依赖于节前胆碱能输入，我们研究了在自发性高血压大鼠（SHR）中观察到的神经活动增加是否可能通过神经节免疫反应性ANF水平反映出来。4周龄的正常血压SHR的腹腔神经节免疫反应性ANF值与Wistar-Kyoto大鼠（WKY）相当。然而，当它们在12周龄时变得高血压时，SHR的腹腔神经节中免疫反应性ANF水平高于WKY组（25.3±2.6对14.5±1.7 pg/神经节；p<0.01），但颈上神经节和结状神经节中的水平没有差异。在8%盐摄入5周的影响下，高血压Dahl盐敏感大鼠腹腔神经节中的值平均增加了四倍，但该组与其盐抵抗同伴之间在任何这些神经节中均未发现差异。正常血压的Sprague-Dawley大鼠在高盐摄入时腹腔和颈上神经节免疫反应性ANF含量高于正常盐摄入时。用醋酸脱氧皮质酮（DOCA）-盐治疗的高血压大鼠和假手术对照组在腹腔神经节中的免疫反应性ANF浓度与在Dahl大鼠中检测到的相似，但同样，两组之间未发现差异。因此，与WKY相比，高血压SHR的腹腔神经节免疫反应性ANF水平更高这一增加是SHR所特有的（尽管所有三种模型在高血压时血浆免疫反应性ANF均升高），并且是腹腔神经节所特有的。（摘要截断于250字）
