Silva Elaine F, Sera Celisa T N, Mourão Aline A, Lopes Paulo R, Moreira Marina C S, Ferreira-Neto Marcos L, Colombari Débora A S, Cravo Sérgio L D, Pedrino Gustavo R
Centre for Neuroscience and Cardiovascular Research, Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás, Goiânia, Goiás, Brazil.
Department of Physiology, Federal University of São Paulo, São Paulo, São Paulo, Brazil.
Clin Exp Pharmacol Physiol. 2015 Nov;42(11):1135-41. doi: 10.1111/1440-1681.12475.
Despite the abundance of evidence that supports the important role of aortic and carotid afferents to short-term regulation of blood pressure and detection of variation in the arterial PO2 , PCO2 and pH, relatively little is known regarding the role of these afferents during changes in the volume and composition of extracellular compartments. The present study sought to determine the involvement of these afferents in the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Sinoaortic-denervated and sham male Wistar rats were anaesthetised with intravenous (i.v.) urethane (1.2 g/kg body weight (bw)) prior to the measurement of the mean arterial pressure (MAP), renal vascular conductance (RVC) and renal sympathetic nerve activity (RSNA). In the sham group, the HS infusion (3 mol/L NaCl, 1.8 mL/kg bw, i.v.) induced transient hypertension (12 ± 4 mmHg from baseline, peak at 10 min; P < 0.05), an increase in RVC (127 ± 9% and 150 ± 13% from baseline, at 20 and 60 min respectively; P < 0.05) and a decrease in RSNA (-34 ± 10% and -29 ± 5% from baseline, at 10 and 60 min respectively; P < 0.05). In sinoaortic-denervated rats, HS infusion promoted a sustained pressor response (30 ± 5 and 17 ± 6 mmHg of baseline values, at 10 and 30 min respectively; P < 0.05) and abolished the increase in RVC (85 ± 8% from baseline, at 10 min) and decrease in RSNA (-4 ± 3% from baseline, at 10 min). These results suggest that aortic and carotid afferents are involved in cardiovascular and renal sympathoinhibition responses induced by acute hypernatremia.
尽管有大量证据支持主动脉和颈动脉传入神经在血压短期调节以及检测动脉血中氧分压、二氧化碳分压和酸碱度变化方面发挥重要作用，但对于这些传入神经在细胞外液容积和成分变化过程中的作用，人们了解得相对较少。本研究旨在确定这些传入神经在高渗盐水（HS）输注诱导的肾血管舒张和交感神经抑制中的作用。在测量平均动脉压（MAP）、肾血管传导性（RVC）和肾交感神经活动（RSNA）之前，用静脉注射（i.v.）乌拉坦（1.2 g/kg体重（bw））对去窦主动脉神经和假手术的雄性Wistar大鼠进行麻醉。在假手术组中，HS输注（3 mol/L NaCl，1.8 mL/kg bw，i.v.）诱导短暂性高血压（比基线升高12±4 mmHg, 10分钟时达到峰值；P<0.05），RVC增加（分别在20分钟和60分钟时比基线增加127±9%和150±13%；P<0.05），RSNA降低（分别在10分钟和60分钟时比基线降低-34±10%和-29±5%；P<0.05）。在去窦主动脉神经的大鼠中，HS输注促进了持续性升压反应（分别在10分钟和30分钟时比基线值升高30±5和17±6 mmHg；P<0.05），并消除了RVC的增加（10分钟时比基线增加85±8%）和RSNA的降低（10分钟时比基线降低-4±3%）。这些结果表明，主动脉和颈动脉传入神经参与了急性高钠血症诱导的心血管和肾交感神经抑制反应。
