Microinjection of resveratrol into rostral ventrolateral medulla decreases sympathetic vasomotor tone through nitric oxide and intracellular Ca2+ in anesthetized male rats
Microinjection of resveratrol into rostral ventrolateral medulla decreases sympathetic vasomotor tone through nitric oxide and intracellular Ca2+ in anesthetized male rats
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DOI：
10.1111/j.1745-7254.2008.00827.x
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发表时间：
2008-08-01
影响因子：
8.2
通讯作者：
Wu, Yu-Ming
中科院分区：
文献类型：
--
作者：
Ma, Hui-Juan;Cao, Ya-Kun;Wu, Yu-Ming
目的：研究白藜芦醇（RES）对血压（BP）、心率（HR）和肾交感神经活动（RSNA）的中枢调节作用。方法：在麻醉大鼠延髓头端腹外侧区（RVLM）微量注射RES，同时记录血压（BP）、心率（HR）和RSNA。结果：RVLM内微量注射RES（20、40和80 μ mol/L，0.2 μ L），可剂量依赖性地降低BP、HR和RSNA。抗雌激素他莫昔芬预处理（100 μ mol/L，0.2 μ L）不影响RES的作用一氧化氮（NO）合酶抑制剂BayK 8644（100 μ mol/L，0.2 μ L）可完全阻断RES的作用（500 nmol/L，0.2 μ L），一种钙通道激动剂，也可以消除RES的作用。预先给予一种有效的酪氨酸磷酸酶抑制剂，原钒酸钠（1 mmol/L，0.2 μ L）可部分减弱RES的抑制作用。结果表明，在RVLM中微量注射RES抑制BP、HR和RSNA。这种作用可能是通过NO合成和Ca 2+内流减少介导的，其中蛋白酪氨酸激酶参与其中。
Aim: To define the effect of resveratrol (RES) on the central regulation of blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA). Methods: RES was microinjected into the rostral ventrolateral medulla (RVLM), and BP, HR, and RSNA were recorded simultaneously in anesthetized rats. Results: A microinjection of RES (20, 40, and 80 mu mol/L, 0.2 mu L) into the RVLM dose dependently decreased BP, HR and RSNA. Pretreatment with an anti-estrogen tamoxifen (100 mu mol/L, 0.2 mu L) did not affect the effects of RES. Pretreatment with N-G-nitro-L-arginine methyl ester (100 mu mol/L, 0.2 mu L), an inhibitor of nitric oxide (NO) synthase, could completely abolish the effect of RES. A prior microinjection of Bay K8644 (500 nmol/L, 0.2 mu L), an agonist of calcium channels, could also abrogate the effect of RES. Prior administration of a potent inhibitor of tyrosine phosphatase, sodium orthovanadate (1 mmol/L, 0.2 mu L), could partially attenuate the inhibitory effect of RES. Conclusion: The results suggest that a microinjection of RES into the RVLM inhibits BP, HR, and RSNA. The effects may be mediated by NO synthesis and a decrease in Ca2+ influx, in which protein tyrosine kinase is involved.