Falcone J C, Granger H J, Meininger G A
Department of Medical Physiology, Texas A&M University, College Station 77843-1114.
Am J Physiol. 1993 Dec;265(6 Pt 2):H1847-55. doi: 10.1152/ajpheart.1993.265.6.H1847.
The purpose of this study was to determine whether the vascular myogenic response is enhanced in hypertension. Experiments were conducted in the intact cremaster muscle microcirculation as well as in isolated arterioles of hypertensive (SHR) and normotensive (WKY) rats. Increasing venous pressure in vivo by approximately 5 mmHg had no effect on normotensive first- (1A) or third-order arteriolar (3A) diameters; in contrast, hypertensive 1A diameter decreased 4% (89 +/- 2 to 85 +/- 3 microns) with an 8% decrease in 3A (24 +/- 2 to 22 +/- 2 microns). To further examine this enhanced constriction to elevated intravascular pressure in SHR, diameter was monitored in isolated 1A during step increases and decreases in intraluminal pressure. Normotensive arterioles displayed myogenic responses between pressures of 50 and 170 cmH2O; in contrast, hypertensive arterioles demonstrated myogenic responses over an extended pressure range (50-210 cmH2O). In addition, the change in diameter for each step change in pressure was greater in the arterioles from SHR, indicating an increased myogenic responsiveness. The myogenic reactions were unaffected by alpha-receptor blockade with phentolamine (10(-6) M), indicating that adrenergic hypersensitivity was not involved in the enhanced response to stretch. Morphometric analysis of the vascular wall revealed no differences in wall thickness, cross-sectional wall area, or wall-to-lumen ratio between normotensive and hypertensive rats. The length-tension relationships for normotensive and hypertensive rats demonstrated that peak active tension occurred at nearly the same vascular smooth muscle length. In addition, SHR arterioles were capable of maintaining higher levels of active tension that WKY arterioles, indicating an altered length-tension curve in chronic arterial hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究的目的是确定高血压时血管肌源性反应是否增强。实验在完整的提睾肌微循环以及高血压(SHR)和正常血压(WKY)大鼠的分离小动脉中进行。体内静脉压升高约5 mmHg对正常血压的一级(1A)或三级小动脉(3A)直径无影响;相比之下,高血压大鼠的1A直径减少了4%(从89±2微米降至85±3微米),3A直径减少了8%(从24±2微米降至22±2微米)。为了进一步研究SHR中这种对血管内压升高的增强收缩作用,在管腔内压力逐步升高和降低期间监测分离的1A的直径。正常血压小动脉在50至170 cmH2O的压力之间表现出肌源性反应;相比之下,高血压小动脉在更宽的压力范围(50 - 210 cmH2O)内表现出肌源性反应。此外,SHR小动脉中压力每步变化时直径的变化更大,表明肌源性反应性增加。肌源性反应不受酚妥拉明(10(-6) M)对α受体的阻断影响,表明肾上腺素能超敏反应不参与对拉伸的增强反应。血管壁的形态计量分析显示,正常血压和高血压大鼠之间在壁厚、横截面积或壁腔比方面没有差异。正常血压和高血压大鼠的长度 - 张力关系表明,峰值主动张力出现在几乎相同的血管平滑肌长度处。此外,SHR小动脉能够维持比WKY小动脉更高水平的主动张力,表明慢性动脉高血压时长度 - 张力曲线发生了改变。(摘要截断于250字)