Department of Pharmacology, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea.
Environ Toxicol Pharmacol. 2005 Feb;19(2):305-11. doi: 10.1016/j.etap.2004.08.002.
Epidemiological studies indicate that arsenic exposure induces hypertension. We hypothesized that arsenate exposure modulates the contractility of vascular smooth muscle through the stress response. Intraperitoneal injection of sodium arsenate (15mg/kg) 16h before increased not only the blood pressure of rats but also the pressor response to preganglionic nerve stimulation (2 and 16Hz) or to bolus injection of vasopressin or phenylephrine in pithed rats as compared with the control rats. Exposure of rat aortic rings to 4mM sodium arsenate for 60min enhanced the contractile responses to KCl or phenylephrine as well as the HSP 70 expression 8h later, but did not affect the relaxation responses to acetylcholine, histamine, or sodium nitroprusside. These results suggest that brief exposure to arsenate is associated with enhanced contractility of vascular smooth muscle through the stress response.
流行病学研究表明，砷暴露会导致高血压。我们假设，砷酸盐暴露通过应激反应调节血管平滑肌的收缩性。与对照组大鼠相比，腹腔注射亚砷酸钠（15mg/kg）16 小时前不仅会增加大鼠的血压，还会增加对节前神经刺激（2 和 16Hz）或加压素或苯肾上腺素的升压反应。暴露于 4mM 亚砷酸钠 60 分钟的大鼠主动脉环增强了对 KCl 或苯肾上腺素的收缩反应，以及 8 小时后 HSP70 的表达，但不影响对乙酰胆碱、组胺或硝普钠的舒张反应。这些结果表明，短暂暴露于砷酸盐会通过应激反应导致血管平滑肌收缩性增强。
