Sandow Shaun L, Bramich Narelle J, Bandi Hari Priya, Rummery Nicole M, Hill Caryl E
Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT, 0200, Australia.
Arterioscler Thromb Vasc Biol. 2003 May 1;23(5):822-8. doi: 10.1161/01.ATV.0000067425.06019.D7. Epub 2003 Mar 20.
To quantify structural and functional characteristics of the caudal artery from spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats with particular reference to endothelium-derived hyperpolarizing factor (EDHF).
Ultrastructural studies showed that the number of myoendothelial gap junctions, smooth muscle cell (SMC) layers, and medial cross-sectional area were significantly greater in SHR than WKY. Intracellular dye labeling demonstrated hyperplasia of SMCs in SHR. Analysis of nerve-mediated excitatory junction potentials recorded in SMCs at the adventitial and luminal borders demonstrated decreased radial coupling of SMCs in SHR. In both SHR and WKY, in the presence of NG-nitro-L-arginine methyl ester and indomethacin, acetylcholine-elicited EDHF was abolished by charybdotoxin and apamin, while iberiotoxin had no effect, implicating the involvement of small and intermediate, but not large, calcium-activated potassium channels. EDHF was abolished by Gap-mimetic peptides, 18beta-glycyrrhetinic acid, and endothelial removal but not affected by the NO scavengers hydroxocobalamin and carboxy-PTIO.
Significant differences in SMC morphology and homocellular and heterocellular coupling exist between the caudal artery of SHR and WKY rats. In the caudal artery of SHR, significantly greater heterocellular coupling compensates for other structural changes in the media to maintain a functional role for EDHF.
量化自发性高血压大鼠（SHR）和正常血压的Wistar Kyoto大鼠（WKY）尾动脉的结构和功能特征，特别关注内皮衍生超极化因子（EDHF）。
超微结构研究表明，SHR的肌内皮间隙连接数量、平滑肌细胞（SMC）层数和中膜横截面积均显著大于WKY。细胞内染料标记显示SHR中SMC增生。对在外膜和管腔边界的SMC中记录的神经介导兴奋性接头电位的分析表明，SHR中SMC的径向耦合降低。在SHR和WKY中，在存在NG-硝基-L-精氨酸甲酯和吲哚美辛的情况下，乙酰胆碱引发的EDHF被大蝎毒素和蜂毒明肽消除，而iberiotoxin没有作用，这表明小和中间钙激活钾通道而非大钙激活钾通道参与其中。EDHF被缝隙模拟肽、18β-甘草次酸和去除内皮消除，但不受NO清除剂羟钴胺和羧基-PTIO的影响。
SHR和WKY大鼠尾动脉的SMC形态以及同细胞和异细胞耦合存在显著差异。在SHR尾动脉中，显著更大的异细胞耦合补偿了中膜的其他结构变化，以维持EDHF的功能作用。
