Neuromolecular mechanisms mediating the effects of chronic intermittent hypoxia on adrenal medulla

• Adrenal catecholamines trigger BP elevation by chronic intermittent hypoxia (CIH).
• CIH increases adrenal catecholamine efflux via up-regulation of Ca2+ signaling.
• CIH dysregulates adrenal HIF-α isoform expression causing oxidative stress.
• CIH-activated carotid body chemoreflex mediates adrenal HIF-α isoform dysregulation.

Sleep disordered breathing (SDB) with recurrent apnea is a major health problem affecting several million adult men and women. Humans with SDB are prone to develop hypertension. Studies on rodents established that exposure to chronic intermittent hypoxia (CIH) alone is sufficient to induce hypertension similar to that seen in patients with SDB. Available evidence from studies on experimental animals suggests that catecholamines secreted from adrenal medulla (AM), an end-organ of the sympathetic nervous system is a major contributor to CIH-induced hypertension. In this article, we present an overview of our current understanding on how CIH reconfigures AM function and highlight recent findings on the underlying cellular and molecular mechanisms.