Abstract
Systemic responses to hypoxia vary among human subjects and in different strains of rats. We examined whether these inherent variations in hypoxic response to carotid body (CB) O2 sensing and involve CO‐H2S signaling. Experiments were performed on age and gender matched Sprague‐Dawley (SD), Brown‐Norway (BN) and Spontaneous Hypertensive (SH) rats. Compared to SD, BN rats exhibited impaired carotid body response to hypoxia, and developed pulmonary edema as a consequence of poor ventilatory adaptation to hypobaric hypoxia. SH rat carotid bodies displayed inherent hypersensitivity to hypoxia and develop hypertension. BN CBs have higher CO and lower H2S levels than SD, while SH carotid bodies have reduced CO and greater H2S generation. Reducing CO levels in BN carotid body increased H2S generation, restoring CB hypoxic sensing and preventing high‐altitude pulmonary edema. Increasing CO levels in SH carotid bodies reduced H2S generation, preventing hypersensitivity to hypoxia and controlling hypertension. Supported by NIH‐HL‐90554.
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