Bund S J
Department of Human Anatomy and Physiology, University College Dublin, Ireland.
J Hypertens. 2000 Sep;18(9):1223-31. doi: 10.1097/00004872-200018090-00008.
The purpose of the study was to test the hypothesis that the increased media thickness: lumen diameter (M:L) ratio of spontaneously hypertensive rat (SHR) resistance arteries effects enhanced arterial contractile responses compared with those of Wistar-Kyoto (WKY) rat normotensive controls under pressurized conditions in vitro.
Contractile responses to the vasoconstrictor agonists noradrenaline and the thromboxane A2 analogue U46619 were assessed in femoral and mesenteric resistance arteries (internal diameters approximately 150 microm) after the development of spontaneous myogenic tone at 100 mmHg and at estimated in vivo pressures.
Arterial contractile responses and structure were assessed in an arteriograph. Relaxed arterial structure was determined by light microscopy. Mean arterial pressure was determined subsequent to femoral artery cannulation.
Under relaxed conditions M:L ratios were significantly greater in SHR arteries at 100 mmHg (P < 0.01) and at in vivo pressures (P<0.01). Myogenic responses were not significantly different between SHR and WKY. Under both pressure conditions the contractile responses of SHR femoral arteries were not significantly different to those of WKY in response to either agonist SHR mesenteric arteries achieved smaller diameters in response to noradrenaline (P<0.05) and U46619 (P<0.05) at 100 mmHg. At in vivo pressures, concentration-response relationships of SHR mesenteric arteries for both agonists were not significantly different compared with those of WKY; however, the maximum percentage reduction of lumen diameter in SHR mesenteric arteries in the presence of noradrenaline was greater than in WKY (P<0.05).
The increased M:L ratio of SHR femoral resistance arteries does not impart an exaggerated contractile function in myogenically active resistance arteries in vitro. For mesenteric arteries the relationship is less clear because increased M:L ratio is associated with increased contractile responses under some, but not all, circumstances.
本研究旨在验证以下假说：在体外加压条件下，与正常血压的Wistar-Kyoto（WKY）大鼠对照相比，自发性高血压大鼠（SHR）阻力动脉中增加的中膜厚度：管腔直径（M:L）比值会增强动脉收缩反应。
在100 mmHg的自发肌源性张力形成后，以及在估计的体内压力下，评估股动脉和肠系膜阻力动脉（内径约150微米）对血管收缩激动剂去甲肾上腺素和血栓素A2类似物U46619的收缩反应。
在血管造影仪中评估动脉收缩反应和结构。通过光学显微镜确定松弛状态下的动脉结构。在股动脉插管后测定平均动脉压。
在松弛条件下，SHR动脉在100 mmHg（P < 0.01）和体内压力（P<0.01）下的M:L比值显著更高。SHR和WKY之间的肌源性反应无显著差异。在两种压力条件下，SHR股动脉对两种激动剂的收缩反应与WKY相比均无显著差异。在100 mmHg时，SHR肠系膜动脉对去甲肾上腺素（P<0.05）和U46619（P<0.05）的反应导致更小的管径。在体内压力下，SHR肠系膜动脉对两种激动剂的浓度-反应关系与WKY相比无显著差异；然而，在去甲肾上腺素存在下，SHR肠系膜动脉管腔直径的最大百分比减小大于WKY（P<0.05）。
SHR股阻力动脉增加的M:L比值在体外对肌源性活跃的阻力动脉并未赋予夸张的收缩功能。对于肠系膜动脉，这种关系不太明确，因为在某些但并非所有情况下，M:L比值增加与收缩反应增加有关。
