Time course of synergistic interaction between DOCA and salt on blood pressure: roles of vasopressin and hepatic osmoreceptors
Time course of synergistic interaction between DOCA and salt on blood pressure: roles of vasopressin and hepatic osmoreceptors
复制标题
DOI：
10.1152/ajpregu.00068.2006
复制
发表时间：
2006-12-01
影响因子：
2.8
通讯作者：
Qi, Yue
中科院分区：
文献类型：
--
作者：
Brooks, Virginia L.;Freeman, Korrina L.;Qi, Yue
DOCA和盐对血压协同作用的时间过程：加压素和肝血管紧张素受体的作用。Am J Physiol Regul Integr Comp Physiol 291：R1825-R1834，2006.首次发表于2006年7月20日; doi：10.1152/ajpregu.00068.2006。在DOCA-盐大鼠中，渗透压和DOCA之间协同相互作用产生高血压的时间过程尚不清楚。因此，在大鼠皮下植入含DOCA（65 mg）或不含药物（假手术）的硅胶颗粒2周后，我们使用遥测压力传感器测定了过量摄入盐（含1% NaCl的饮用水）2周期间的血压（BP）和心率（HR）反应。增加盐浓度后，假手术大鼠的血压没有变化，但DOCA大鼠的血压在4小时内升高。初始高血压30-35 mmHg在2天内稳定，5天后进一步升高至30 mmHg。HR首先在黑暗阶段下降;第二阶段与HR和BP变异性突然增加和HR变异性降低有关。DOCA处理的大鼠通过加压素和非加压素机制对急性静脉高渗盐水输注的升压反应加倍。仅在DOCA处理的大鼠中，门静脉高渗盐水输注增加BP，这被V-1加压素阻断所阻止。DOCA盐2周后，口服水迅速降低血压。门静脉内灌注水并不能降低DOCA盐大鼠的血压，这表明肝脏的β受体没有参与。总之，摄入过量盐的DOCA治疗大鼠的高血压表现出多个阶段，并且可以迅速逆转。高渗诱导的血管加压素和非血管加压素升压机制，DOCA增强，肝垂体后叶素受体可能有助于初始发育阶段。随着时间的推移，DOCA-盐的组合诱导自主神经系统调节的显著变化，这可能有利于高血压的发展。
Time course of synergistic interaction between DOCA and salt on blood pressure: roles of vasopressin and hepatic osmoreceptors. Am J Physiol Regul Integr Comp Physiol 291: R1825-R1834, 2006. First published July 20, 2006; doi:10.1152/ajpregu.00068.2006.- In DOCA-salt rats, the time course of the synergistic interaction between osmolality and DOCA to produce hypertension is unknown. Therefore, in rats 2 wk after implantation of subcutaneous silicone pellets containing DOCA (65 mg) or no drug (sham), we determined blood pressure (BP) and heart rate (HR) responses, using telemetric pressure transducers, during 2 wk of excess salt ingestion (1% NaCl in drinking water). BP was unaltered in sham rats after increased salt, but in DOCA rats BP increased within 4 h. The initial hypertension of 30-35 mmHg stabilized within 2 days, followed similar to 5 days later by a further increment of similar to 30 mmHg. HR first decreased during the dark phase; the second phase was linked to an abrupt increase in HR and BP variability and decreased HR variability. Pressor responses to acute intravenous hypertonic saline infusion were doubled in DOCA-treated rats via vasopressin and nonvasopressin mechanisms. Only in DOCA-treated rats, portal vein hypertonic saline infusion increased BP, which was prevented by V-1 vasopressin blockade. After 2 wk of DOCA-salt, oral ingestion of water rapidly decreased BP. Intraportal infusion of water did not lower BP in DOCA-salt rats, suggesting that hepatic osmoreceptors were not involved. In summary, the hypertension of DOCA-treated rats consuming excess salt exhibits multiple phases and can be rapidly reversed. Hypertonicity-induced vasopressin and nonvasopressin pressor mechanisms that are augmented by DOCA, and hepatic osmoreceptors may contribute to the initial developmental phase. With time, combined DOCA-salt induces marked changes in the regulation of the autonomic nervous system, which may favor hypertension development.