Xiang Lusha, Naik Jay S, Hodnett Benjamin L, Hester Robert L
Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216-4505, USA.
Am J Physiol Regul Integr Comp Physiol. 2006 Jan;290(1):R134-8. doi: 10.1152/ajpregu.00295.2005. Epub 2005 Sep 15.
These studies tested the hypothesis that in obese Zucker rats (OZRs), a model of metabolic syndrome, the impaired functional vasodilation is due to increased thromboxane receptor (TP)-mediated vasoconstriction and/or decreased prostacyclin-induced vasodilation. Spinotrapezius arcade arterioles from 12-wk-old lean (LZR) and OZR were chosen for microcirculatory observation. Arteriolar diameter (5 LZR and 6 OZR) was measured after 2 min of muscle stimulation in the absence or presence of 1 microM SQ-29548 (TP antagonist). Additionally, arteriolar diameter (6 for each group) was measured after application of iloprost (prostacyclin analog; 0.28, 2.8, and 28 microM), arachidonic acid (10 microM), and sodium nitroprusside (0.1, 1, and 10 microM) in the absence or presence of 1 microM SQ-29548. A 10 microM concentration of adenosine was used to induce a maximal dilation. Basal diameters were not different between LZRs and OZRs. Functional hyperemia and arachidonic acid-mediated vasodilations were significantly attenuated in OZR compared with LZR, and treatment with 1 microM SQ-29548 significantly enhanced the dilations in OZRs, although it had no effect in LZRs. Vasodilatory responses to iloprost and sodium nitroprusside (1 and 10 microM) were significantly reduced in OZR. Adenosine-mediated vasodilation was not different between groups. These results suggest that the impaired functional dilation in the OZR is due to an increased TP-mediated vasoconstriction and a decreased PGI2-induced vasodilation.
在肥胖Zucker大鼠（OZR）这一代谢综合征模型中，功能性血管舒张受损是由于血栓素受体（TP）介导的血管收缩增加和/或前列环素诱导的血管舒张减少所致。选取12周龄的瘦素受体（LZR）大鼠和OZR大鼠的斜方肌弓状小动脉进行微循环观察。在不存在或存在1微摩尔SQ - 29548（TP拮抗剂）的情况下，对肌肉进行2分钟刺激后，测量小动脉直径（5只LZR大鼠和6只OZR大鼠）。此外，在不存在或存在1微摩尔SQ - 29548的情况下，应用伊洛前列素（前列环素类似物；0.28、2.8和28微摩尔）、花生四烯酸（10微摩尔）和硝普钠（0.1、1和10微摩尔）后，测量小动脉直径（每组6只）。使用10微摩尔浓度的腺苷诱导最大舒张。LZR大鼠和OZR大鼠的基础直径无差异。与LZR大鼠相比，OZR大鼠的功能性充血和花生四烯酸介导的血管舒张明显减弱，用1微摩尔SQ - 29548处理可显著增强OZR大鼠的舒张，尽管对LZR大鼠无影响。OZR大鼠对伊洛前列素和硝普钠（1和10微摩尔）的血管舒张反应明显降低。各组之间腺苷介导的血管舒张无差异。这些结果表明，OZR大鼠功能性舒张受损是由于TP介导的血管收缩增加和前列环素I2（PGI2）诱导的血管舒张减少所致。
