Sakai Y, Inazu M
2nd Department of Physiology, Showa University, School of Medicine, Tokyo, Japan.
Eur J Pharmacol. 1991 Aug 6;200(2-3):227-31. doi: 10.1016/0014-2999(91)90576-c.
We investigated the hypertensive changes in renal arteries isolated from 21-week-old spontaneously hypertensive rats (SHR), and from age-matched normotensive Wistar-Kyoto rats (WKY). The maximum contraction of renal arteries from SHR in response to norepinephrine (NE), serotonin (5-HT) and KCl was greater than that of arteries from WKY. The threshold and EC50 concentrations of NE, 5-HT and KCl were not significantly different between SHR and WKY. Contraction induced by removal of K+ was inhibited by 10(-8) M prazosin. Less than 10(-7) M NE in K(+)-free solution did not cause contraction. Addition of 5.9 mM KCl to K(+)-free solution in the presence of 10(-5) M NE induced relaxation, which was followed by contraction to about the same level as that before KCl addition. The duration of the K(+)-induced relaxation in SHR (22.4 +/- 0.9 min) was slightly, but significantly shorter than that in WKY (26.6 +/- 0.8 min) arteries. In K(+)-free solution with reduced Na+, the duration of the relaxation induced by KCl was shorter than that in the normal solution, for both SHR (13.8 +/- 0.3 min) and WKY (14.1 +/- 0.5 min). Such differences could be caused by increased influx and decreased efflux of Ca2+, which depend on the Na+ concentration and are related to the Na(+)-Ca2+ exchange. The results suggest that enhanced renal vascular reactivity in hypertension may depend on structural changes and increased Na+ pump activity.
我们研究了从21周龄自发性高血压大鼠（SHR）以及年龄匹配的正常血压Wistar-Kyoto大鼠（WKY）分离出的肾动脉中的高血压变化。SHR肾动脉对去甲肾上腺素（NE）、5-羟色胺（5-HT）和氯化钾（KCl）的最大收缩反应大于WKY的动脉。SHR和WKY之间，NE、5-HT和KCl的阈值浓度和半数有效浓度（EC50）没有显著差异。去除钾离子（K+）诱导的收缩可被10^(-8) M哌唑嗪抑制。在无钾溶液中，低于10^(-7) M的NE不会引起收缩。在存在10^(-5) M NE的无钾溶液中加入5.9 mM KCl会诱导舒张，随后收缩至与添加KCl前大致相同的水平。SHR中K+诱导的舒张持续时间（22.4±0.9分钟）略短，但显著短于WKY动脉中的舒张持续时间（26.6±0.8分钟）。在钠离子（Na+）减少的无钾溶液中，SHR（13.8±0.3分钟）和WKY（14.1±0.5分钟）中KCl诱导的舒张持续时间均短于正常溶液中的舒张持续时间。这种差异可能是由钙离子（Ca2+）内流增加和外流减少引起的，这取决于Na+浓度，并且与钠钙交换有关。结果表明，高血压中肾血管反应性增强可能取决于结构变化和钠泵活性增加。
