Role of endogenous carbon monoxide in central regulation of arterial pressure
Role of endogenous carbon monoxide in central regulation of arterial pressure
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DOI：
10.1161/01.hyp.30.4.962
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发表时间：
1997-10-01
期刊：
影响因子：
8.3
通讯作者：
Nasjletti, A
中科院分区：
文献类型：
--
作者：
Johnson, RA;Colombari, E;Nasjletti, A
我们研究了内源性一氧化碳合成抑制剂deuteroporphyrin 2,4-双乙二醇锌（ZnDPBG）引起动脉血压升高的神经机制的贡献。通过分析注射苯肾上腺素或硝普钠改变动脉压时动脉压-心率的关系，观察ZnDPBG （45 μ mol/kg IP）预处理和未处理大鼠动脉压感受反射对心率的控制。ZnDPBG使动脉压从110+/-3增加到126+/-2 mm Hg，而不引起心动过缓。ZnDPBG治疗降低了心率对动脉压变化反应的最大增益（-1.9+/-0.3 vs -4.8+/-1.0 bpm/mm Hg）。通过比较ZnDPBG （45 μ mol/kg IP）对主动脉去神经和非主动脉去神经大鼠的压力反应，探讨了ZnDPBG通过减弱压力感受反射功能而升高动脉压力的可能性。ZnDPBG在动脉压力感受器失传入和非动脉压力感受器失传入大鼠中的加压作用相似，这意味着压力的增加不仅仅是压力感受器反射功能减弱的结果。ZnDPBG （1 nmol / 100 nL）注射到大鼠的NTS后，使动脉压从111+/-4 mmhg升高到126+/-5 mmhg，并通过在NTS中同侧微量注射一氧化碳逆转了这种作用。因此，ZnDPBG的升压作用可能依赖于抑制NTS中一氧化碳的产生。这说明脑血红素加氧酶形成的一氧化碳在动脉压的中枢调节中起作用。
We investigated the contribution of neural mechanisms to the arterial pressure increase produced by zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG), an inhibitor of endogenous carbon monoxide synthesis. The arterial baroreceptor reflex control of heart rate was examined in rats with and without ZnDPBG pretreatment (45 mu mol/kg IP) by analysis of the arterial pressure-heart rate relationship during infusions of phenylephrine or sodium nitroprusside to vary arterial pressure. ZnDPBG increased arterial pressure from 110+/-3 to 126+/-2 mm Hg without eliciting bradycardia. The maximum gain of the heart rate response to changes in arterial pressure was attenuated by ZnDPBG treatment (-1.9+/-0.3 versus -4.8+/-1.0 bpm/mm Hg). The possibility that ZnDPBG elevates arterial pressure by attenuating baroreceptor reflex function was addressed by comparing the presser response to ZnDPBG (45 mu mol/kg IP) in rats with and without sinoaortic denervation. The presser effect of ZnDPBG was similar in rats with and without arterial baroreceptor deafferentation, implying that the increase in pressure is nat simply the consequence of attenuated baroreceptor reflex function per se. The possibility that ZnDPBG increases arterial pressure via an effect on the nucleus tractus solitarii (NTS) also was investigated ZnDPBG (1 nmol in 100 nL) injected into the NTS of rats increased arterial pressure from 111+/-4 to 126+/-5 mm Hg, and this effect was reversed by an ipsilateral microinjection of carbon monoxide into the NTS. Accordingly, the pressor effect of ZnDPBG may rely on inhibition of carbon monoxide production in the NTS. This implies that carbon monoxide formed by brain heme oxygenase plays a role in the central regulation of arterial pressure.