Collis M G, DeMey C, Vanhoutte P M
Hypertension. 1980 Jan-Feb;2(1):45-52. doi: 10.1161/01.hyp.2.1.45.
The renal resistance vessels of the mature spontaneously hypertensive rat (SHR) exhibit increased reactivity to vasoconstrictor agonists. This could be a cause or consequence of hypertension. We have compared vascular reactivity in isolated perfused kidneys from 46-day-old SHR and from normotensive control rats. The amplitude of responses in kidneys from the SHR to angiotensin II, barium chloride, or norepinephrine was not different from the control. Therefore, increased reactivity of the renal vascular smooth muscle cannot be an early pathogenic mechanism in spontaneous hypertension. Responses evoked by 5-hydroxytryptamine (serotonin) were of a greater amplitude in the SHR than in the control kidney. However, this difference was due to an interaction of serotonin with the sympathetic nerves, as it was abolished by treatment of the rats with 6-hydroxydopamine. Responses induced by electrical stimulation of the renal sympathetic nerves were also of greater amplitude in SHR than in control kidneys, both before and after the blockade of norepinephrine disposition mechanisms. Nerve stimulation evoked a greater efflux of endogenous norepinephrine from kidneys of the SHR than from those of control rats. Thus, the increased reactivity of the SHR kidney to renal nerve stimulation is due to an augmented release of endogenous norepinephrine. This could be an important factor in the early development of hypertension.
成熟的自发性高血压大鼠（SHR）的肾阻力血管对血管收缩剂激动剂的反应性增强。这可能是高血压的原因或结果。我们比较了46日龄SHR和正常血压对照大鼠的离体灌注肾脏的血管反应性。SHR肾脏对血管紧张素II、氯化钡或去甲肾上腺素的反应幅度与对照组无差异。因此，肾血管平滑肌反应性增加不可能是自发性高血压的早期致病机制。5-羟色胺（血清素）在SHR中引起的反应幅度大于对照肾脏。然而，这种差异是由于血清素与交感神经的相互作用所致，因为用6-羟基多巴胺处理大鼠后这种差异消失了。在去甲肾上腺素处置机制被阻断之前和之后，电刺激肾交感神经在SHR中诱导的反应幅度也大于对照肾脏。神经刺激引起SHR肾脏内源性去甲肾上腺素的流出量大于对照大鼠。因此，SHR肾脏对肾神经刺激反应性增加是由于内源性去甲肾上腺素释放增加所致。这可能是高血压早期发展的一个重要因素。
