Minson J, Arnolda L, Llewellyn-Smith I, Pilowsky P, Chalmers J
Department of Medicine, Flinders University of South Australia, Adelaide.
Hypertension. 1996 Mar;27(3 Pt 1):433-41. doi: 10.1161/01.hyp.27.3.433.
Neurons immunoreactive for Fos, the protein product of the immediate early gene c-fos, have been compared in the rostral ventral medulla and spinal cord of conscious normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) after baroreceptor unloading. Hypotension induced by a 60-minute intravenous infusion of sodium nitroprusside reduced baroreceptor activity; controls received intravenous saline. In WKY, 474 +/- 56 (n=6) Fos-positive neurons were identified in the rostral ventral medulla after nitroprusside infusion, a fivefold increase from controls; 50% of the tyrosine hydroxylase-containing neurons in the rostral ventral medulla were activated by this hypotension. Sympathetic preganglionic neurons, mainly sympathoadrenal neurons, were Fos positive after nitroprusside, but Fos-positive sympathetic preganglionic neurons were not observed in control WKY. In SHR, Fos immunoreactivity in the rostral ventral medulla was elevated in the control group compared with the WKY controls (236 +/- 31 and 93 +/- 15, respectively, n=6 for both). Nitroprusside hypotension did not further increase Fos immunoreactivity in the rostral ventral medulla, although the number of Fos-positive spinal sympathetic neurons increased. Our results have identified different neuronal activities between WKY and SHR in sites that are critical to sympathetic outflow. In WKY, nitroprusside effects are consistent with an activation of rostral ventral medulla neurons, including bulbospinal neurons, that are normally inhibited by baroreceptor activity. In SHR, basal nerve activity is increased, so even at rest, rostral ventral medulla neurons and sympathetic preganglionic neurons, mainly sympathoadrenal neurons, are Fos immunoreactive. These activated neurons are likely to contribute to the elevated blood pressure in this rat strain.
在压力感受器卸载后，对清醒的正常血压Wistar-Kyoto大鼠（WKY）和自发性高血压大鼠（SHR）的延髓腹侧头端和脊髓中，对即刻早期基因c-fos的蛋白质产物Fos免疫反应阳性的神经元进行了比较。通过静脉输注硝普钠60分钟诱导的低血压降低了压力感受器活性；对照组接受静脉生理盐水输注。在WKY中，输注硝普钠后，在延髓腹侧头端鉴定出474±56（n = 6）个Fos阳性神经元，比对照组增加了五倍；延髓腹侧头端中50%含酪氨酸羟化酶的神经元被这种低血压激活。交感神经节前神经元，主要是交感肾上腺神经元，在输注硝普钠后Fos呈阳性，但在对照WKY中未观察到Fos阳性的交感神经节前神经元。在SHR中，与WKY对照组相比，对照组延髓腹侧头端的Fos免疫反应性升高（分别为236±31和93±15，n = 6）。硝普钠诱导的低血压并没有进一步增加延髓腹侧头端的Fos免疫反应性，尽管Fos阳性的脊髓交感神经元数量增加。我们的结果确定了WKY和SHR在对交感神经输出至关重要的部位存在不同的神经元活动。在WKY中，硝普钠的作用与延髓腹侧头端神经元（包括延髓脊髓神经元）的激活一致，这些神经元通常受到压力感受器活动的抑制。在SHR中，基础神经活动增加，因此即使在休息时，延髓腹侧头端神经元和交感神经节前神经元（主要是交感肾上腺神经元）Fos免疫反应阳性。这些激活的神经元可能导致该大鼠品系血压升高。
