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- W2296936004 abstract "Conditioning with chronic intermittent hypoxia (CIH) causes hypertension associated with elevated sympathetic nerve activity and increased cardiorespiratory sensitivity to hypoxia. Hypoxia sensed by the carotid bodies drives cardiorespiratory regulating sites, including the PVN via the nucleus tractus solitarius. Our hypothesis is that CIH-conditioning alters the balance of excitatory and inhibitory influences on CR control via the PVN. Male SD rats were exposed to CIH for 8 h/day for 10 days. Blood pressure (BP), heart rate (HR), diaphragm (DEMG) and genioglossus (GGEMG) activity were recorded in anesthetized, ventilated and vagotomized rats. The PVN was disinhibited by injecting bicuculline (BIC, a GABAA receptor antagonist, 100 pmol) before and after blocking AVP receptors in the RVLM with SR49059 (200 pmol/side, bilateral). In control rats, BIC increased BP, HR, minute DEMG and GGEMG. Following RVLM blockade, these variables were significantly decreased (p < 0.05). Although more pronounced, similar responses were observed in CIH-conditioned rats; however, it required a higher dose of blocker (400 pmol/side, bilateral) to blunt the effect (p < 0.05). These finding suggests that AVP modulates cardiorespiratory output via the RVLM and CIH-conditioned rats show augmented AVP transmission, suggesting AVP as a candidate neuropeptide that controls sympathetic tone and respiratory output during CIH. Supported by: HL 87620." @default.
- W2296936004 created "2016-06-24" @default.
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- W2296936004 date "2009-04-01" @default.
- W2296936004 modified "2023-09-27" @default.
- W2296936004 title "Increased vasopressin transmission from the hypothalamic paraventricular nucleus (PVN) to the rostroventrolateral medulla (RVLM) augments cardiorespiratory outflow in CIH‐conditioned rats" @default.
- W2296936004 doi "https://doi.org/10.1096/fasebj.23.1_supplement.1009.1" @default.
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