Effect of felodipine on blood pressure and vascular reactivity in stroke-prone spontaneously hypertensive rats.
Effect of felodipine on blood pressure and vascular reactivity in stroke-prone spontaneously hypertensive rats.
复制标题
非洛地平对易发生卒中的自发性高血压大鼠血压和血管反应性的影响。
DOI：
10.1097/00004872-198901000-00005
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发表时间：
1989
影响因子：
4.9
通讯作者：
Webb,RC
中科院分区：
文献类型：
--
作者：
Bruner,CA;Webb,RC
易卒中自发性高血压大鼠(SHRSP)的分离尾动脉对去甲肾上腺素的反应表现出振荡收缩，而正常血压的Wistar-京都大鼠(WKY)则不是。以前的研究表明，这些振荡的机制涉及膜上钙和/或钾处理的改变，这种血管变化是SHRSP中与高血压相关的遗传缺陷。本实验的目的是确定钙通道阻滞剂非洛地平治疗SHRSP是否会改变振荡活动。成年SHRSP和WKY大鼠口服非洛地平8周。非洛地平治疗可显著降低SHRSP的血压(对照组SHRSP：240+/-7 mm Hg，n=6；非洛地平组SHRSP：164+/-8 mm Hg，n=5，P<；0.05；尾袖法)。将所有大鼠螺旋切断的尾动脉条固定在组织浴中，记录等长力，并以每个浓度的去甲肾上腺素(6×10~(-9)~6×10~(-6)mol/L)作用20min。振荡活动被定义为在去甲肾上腺素孵育的最后10分钟内发生的所有时相收缩幅度的总和。与对照组相比，非洛地平治疗的SHRSP尾动脉的振荡活动明显减少。当直接加入组织浴中时，非洛地平也能抑制振荡活动。因此，似乎非洛地平可以降低SHRSP的血压，至少部分是通过纠正导致振荡活动的遗传缺陷来实现的。
Isolated tail arteries from stroke-prone spontaneously hypertensive rats (SHRSP), but not from normotensive Wistar-Kyoto rats (WKY), exhibit oscillatory contractions in response to norepinephrine. Previous studies indicate that the mechanism for these oscillations involves altered membrane calcium and/or potassium handling, and that this vascular change is a genetic defect associated with hypertension in SHRSP. The purpose of this experiment was to determine whether treatment of SHRSP with the calcium entry blocker felodipine would alter oscillatory activity. Adult SHRSP and WKY rats were treated orally with felodipine for 8 weeks. Felodipine treatment produced a significant decrease in blood pressure in SHRSP (control SHRSP: 240+/-7 mmHg, n= 6; felodipine-treated SHRSP: 164+/-8 mmHg, n= 5, P< 0.05; tail-cuff method). Helically-cut tail artery strips from all rats were mounted in tissue baths for isometric force recording and exposed to norepinephrine (6 x 10-9 to 6 x 10-6mol/l) for 20min at each concentration. Oscillatory activity was defined as the sum of the magnitudes of all phasic contractions occurring during the final 10min of norepinephrine incubation. Oscillatory activity was markedly reduced in tail arteries from felodipine-treated SHRSP when compared with control SHRSP. Felodipine also inhibited oscillatory activity when added directly to the tissue bath. It seems, therefore, that felodipine may lower blood pressure in SHRSP, at least in part, by correcting the genetic defect responsible for oscillatory activity