engleski

Changes in renal sympathetic nerve activity during and after exposure to acute intermittent hypercapnia

Elevated levels of carbon dioxide (hypercapnia) and/or decreased level of oxygen (hypoxia) act through neural networks to influence ventilatory and cardiovascular function. Both hypercapnic and hypoxic stimuli can evoke increase in sympathetic nerve activity and it appears that hypoxia can evoke prolonged duration of this increase. The present study was performed to investigate the renal sympathetic nerve activity in urethane-anesthetized, mechanically ventilated Sprague-Dawley rats exposed to five hypercapnic stimuli each lasting 3 minutes. Blood pressure and renal sympathetic nerve activity were measured and recorded throughout the experiment. Analysis was performed in the period before and during hypercapnic exposures (15% of the CO2 in the air), as well as 15, 30 and 60 minutes after the last hypercapnic episode. Renal sympathetic nerve activity increased to 190.3±22.8% during hypercapnia when compared to baseline. At 15 minutes after the last hypercapnic exposure nerve activity remained elevated at 138.0±14.8%. At 30 and 60 minutes renal sympathetic nerve activity was 136.8±21.5% and 131.8±18.3%, respectively. Acute intermittent hypercapnia evoked increase in renal sympathetic nerve activity that lasted at least 60 minutes after cessation of stimulus.

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