Medullary Respiratory Network Drives Sympathetic Overactivity and Hypertension in Rats Submitted to Chronic Intermittent Hypoxia
Why should researchers in charge of basic and clinical investigation of hypertension also pay attention to respiration? More than its primary role to orchestrate the diaphragm, chest, and abdominal muscle contraction and relaxation, essential for O2 and CO2 pulmonary exchanges, the brain stem respiratory network is also precise and timely connected with the presympathetic neurons located in the ventral medulla. This central respiratory–sympathetic interaction is thought to closely match cardiac output and tissue perfusion with minute ventilation to optimize blood gases exchange according to the metabolic demand. Recent data on models of hypertension induced by chronic intermittent hypoxia, a well-accepted experimental model to study the mechanisms underpinning hypertension observed in obstructive sleep apnea patients, showed that sympathetic-dependent hypertension is accompanied by clear changes in the neural respiratory network activity and its coupling with the sympathetic nervous system. In this review, we present recent experimental evidence indicating that changes in the respiratory–sympathetic coupling mechanisms should be considered as a novel and relevant player underpinning neurogenic hypertension. In perspective, we are suggesting that respiratory dysfunction might be one of the unrevealed causes of the hypertension, and it is plausible to be taken into consideration that maneuvers including the control of respiratory activity could be considered as an alternative strategy to manage the sympathetic overactivity in different neurogenic hypertensive states.
- Received May 22, 2012.
- Revision received June 13, 2012.
- Accepted September 14, 2012.
- © 2012 American Heart Association, Inc.