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下丘脑去甲肾上腺素释放及去窦弓神经大鼠对氯化钠的心血管反应。

Hypothalamic NE release and cardiovascular response to NaCl in sinoaortic-denervated rats.

作者信息

Nakata T, Berard W, Kogosov E, Alexander N

机构信息

Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.

出版信息

Am J Physiol. 1991 Apr;260(4 Pt 2):R733-8. doi: 10.1152/ajpregu.1991.260.4.R733.

DOI:10.1152/ajpregu.1991.260.4.R733
PMID:1672796
Abstract

We determined the activity of noradrenergic neurons in the nucleus of the posterior hypothalamus (PH) of sinoaortic-denervated (SAD) and sham-operated (SO) rats during cardiovascular responses to intravenous (iv) or local brain dialysis of NaCl. PH extracellular norepinephrine (NE) was collected by microdialysis from freely moving rats, and dialysate NE was measured by radioenzymatic assay. Three days after SAD or SO, mean arterial pressure (MAP) and heart rate (HR) were significantly higher in SAD rats than SO rats. Basal levels of PH dialysate were also significantly elevated in SAD rats. Local dialysis of PH with hypertonic NaCl produced pressor and tachycardiac responses coupled with increased NE release in PH in both groups, but the increases in MAP and dialysate NE were larger in SAD than SO rats. Ganglionic blockade with iv hexamethonium elicited significantly larger depressor and bradycardiac responses in SAD rats, whereas the percent increase of dialysate NE was smaller than that of SO rats. The iv infusion of hypertonic NaCl produced larger pressor responses in SAD than SO rats and a significant increase in dialysate NE from PH of SAD but not SO rats. These findings indicate that 1) PH is an important site of NaCl action and 2) noradrenergic input in PH receives tonic inhibitory input from baroreflex pathways and contributes to cardiovascular hyperactivity and hypertension in SAD rats.

摘要

我们测定了经 sinoaortic 去神经支配(SAD)和假手术(SO)处理的大鼠在对静脉注射(iv)或局部脑内透析 NaCl 产生心血管反应期间,下丘脑后部(PH)核团中去甲肾上腺素能神经元的活性。通过微透析从自由活动的大鼠中收集 PH 细胞外去甲肾上腺素(NE),并通过放射酶法测定透析液中的 NE。在 SAD 或 SO 处理三天后,SAD 大鼠的平均动脉压(MAP)和心率(HR)显著高于 SO 大鼠。SAD 大鼠 PH 透析液的基础水平也显著升高。两组中,用高渗 NaCl 对 PH 进行局部透析均产生升压和心动过速反应,并伴有 PH 中 NE 释放增加,但 SAD 大鼠的 MAP 和透析液 NE 的升高幅度大于 SO 大鼠。静脉注射六甲铵进行神经节阻断在 SAD 大鼠中引起显著更大的降压和心动过缓反应,而透析液 NE 的增加百分比小于 SO 大鼠。静脉输注高渗 NaCl 在 SAD 大鼠中产生的升压反应大于 SO 大鼠,且 SAD 大鼠而非 SO 大鼠的 PH 透析液 NE 显著增加。这些发现表明:1)PH 是 NaCl 作用的重要部位;2)PH 中的去甲肾上腺素能输入接受来自压力反射通路的紧张性抑制输入,并促成 SAD 大鼠的心血管活动亢进和高血压。

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