Chronic intermittent hypoxia (CIH) enhances the lumbar sympathoexcitatory response to central hyperosmotic NaCl

Abstract

Rats exposed to CIH develop elevated mean arterial pressure (MAP) and sympathetic nerve activity (SNA). Although pro-hypertensive factors such as stress and obesity have been implicated in responses to CIH, little is known regarding interactions of CIH with central effects of Na/osmolality. To investigate this issue, rats were exposed to alternating 3 min periods of normoxia (room air, 21% O2) and hypoxia (10% O2) for 8 hr/day for 7 days. Control rats continuously breathed normoxic air. Rats were then anesthetized and responses of MAP, renal and lumbar SNA to internal carotid artery injection (100 μl) of isotonic (150 mM) and hypertonic (450 mM) NaCl solutions were recorded. In control (n=7) and CIH-exposed (n=7) rats, ICA injection of isotonic NaCl was without effect on all recorded variables. In contrast, ICA injection of hypertonic NaCl significantly increased MAP (P<0.01), renal SNA (P<0.01–0.001) and lumbar SNA (P<0.01–0.001) in control and CIH-exposed rats. When compared across groups, the magnitude of MAP (control: 36±4 mmHg, CIH: 33±4 mmHg) and renal SNA (control: 191±12%, CIH: 194±16%) responses were similar. In contrast, the increase in lumbar SNA was significantly (P<0.05) greater in CIH-exposed (213±32%) rats compared to controls (153±8%). These data suggest that exaggerated sympathetic outflow following CIH may involve central interactions with Na/hyperosmolality. Specifically, CIH may sensitize those neural elements responsive to Na/hyperosmolality that regulate lumbar SNA. Support: HL071645 (GMT), HL66335 (SWM)