Janssen B J, Leenders P J, Smits J F
Department of Pharmacology, Cardiovascular Research Institute Maastricht, Universiteit Maastricht, Maastricht 6200 MD, The Netherlands.
Am J Physiol Regul Integr Comp Physiol. 2000 Jan;278(1):R215-25. doi: 10.1152/ajpregu.2000.278.1.R215.
Knowledge on murine blood pressure and heart rate control mechanisms is limited. With the use of a tethering system, mean arterial pressure (MAP) and pulse interval (PI) were continuously recorded for periods up to 3 wk in Swiss mice. The day-to-day variation of MAP and PI was stable from 5 days after surgery. Within each mouse (n = 9), MAP and PI varied by 21+/-6 mm Hg and 17+/-4 ms around their respective 24-h averages (97+/-3 mm Hg and 89+/-3 ms). Over 24-h periods, MAP and PI were bimodally distributed and clustered around two preferential states. Short-term variability of MAP and PI was compared between the resting (control) and active states using spectral analysis. In resting conditions, variability of MAP was mainly confined to frequencies <1 Hz, whereas variability of PI was predominantly linked to the respiration cycle (3-6 Hz). In the active state, MAP power increased in the 0.08- to 3-Hz range, whereas PI power fell in the 0.08- to 0.4-Hz range. In both conditions, coherence between MAP and PI was high at 0.4 Hz with MAP leading the PI fluctuations by 0.3-0.4 s, suggesting that reflex coupling between MAP and PI occurred at the same frequency range as in rats. Short-term variability of MAP and PI was studied after intravenous injection of autonomic blockers. Compared with the resting control state, MAP fell and PI increased after ganglionic blockade with hexamethonium. Comparable responses of MAP were obtained with the alpha-blocker prazosin, whereas the beta-blocker metoprolol increased PI similarly. Muscarinic blockade with atropine did not significantly alter steady-state levels of MAP and PI. Both hexamethonium and prazosin decreased MAP variability in the 0.08- to 1-Hz range. In contrast, after hexamethonium and metoprolol, PI variability increased in the 0.4- to 3-Hz range. Atropine had no effect on MAP fluctuations but decreased those of PI in the 0.08- to 1-Hz range. These data indicate that, in mice, blood pressure and its variability are predominantly under sympathetic control, whereas both vagal and sympathetic nerves control PI variability. Blockade of endogenous nitric oxide formation by N(G)-nitro-L-arginine methyl ester increased MAP variability specifically in the 0.08- to 0.4-Hz range, suggesting a role of nitric oxide in buffering blood pressure fluctuations.
关于小鼠血压和心率控制机制的知识有限。利用一种系留系统，在瑞士小鼠中连续记录平均动脉压（MAP）和脉搏间期（PI）长达3周。术后5天起，MAP和PI的每日变化稳定。在每只小鼠（n = 9）中，MAP和PI围绕其各自的24小时平均值（97±3 mmHg和89±3 ms）分别变化21±6 mmHg和17±4 ms。在24小时期间，MAP和PI呈双峰分布，并聚集在两种优先状态周围。使用频谱分析比较静息（对照）状态和活动状态下MAP和PI的短期变异性。在静息条件下，MAP的变异性主要局限于频率<1 Hz，而PI的变异性主要与呼吸周期（3 - 6 Hz）相关。在活动状态下，MAP功率在0.08至3 Hz范围内增加，而PI功率在0.08至0.4 Hz范围内下降。在两种条件下，MAP和PI在0.4 Hz时的相干性都很高，MAP的波动比PI超前0.3 - 0.4秒，这表明MAP和PI之间的反射耦合发生在与大鼠相同的频率范围内。静脉注射自主神经阻滞剂后研究了MAP和PI的短期变异性。与静息对照状态相比，用六甲铵进行神经节阻滞后MAP下降而PI增加。用α受体阻滞剂哌唑嗪可获得类似的MAP反应，而β受体阻滞剂美托洛尔同样增加PI。用阿托品进行毒蕈碱阻断并未显著改变MAP和PI的稳态水平。六甲铵和哌唑嗪均降低了0.08至1 Hz范围内的MAP变异性。相反，在使用六甲铵和美托洛尔后，PI变异性在0.4至3 Hz范围内增加。阿托品对MAP波动无影响，但降低了0.08至1 Hz范围内的PI波动。这些数据表明，在小鼠中，血压及其变异性主要受交感神经控制，而迷走神经和交感神经均控制PI变异性。用N(G)-硝基-L-精氨酸甲酯阻断内源性一氧化氮形成会特异性增加0.08至0.4 Hz范围内的MAP变异性，这表明一氧化氮在缓冲血压波动中起作用。
