Environmental Stress, Hypoventilatory Breathing and Blood Pressure Regulation

Summary

Research in our laboratory is based on the hypothesis that chronic breathing suppression associated with stressful environments can contribute to high blood pressure via its effects on pCO₂, acid-base balance, and renal regulation of sodium. This hypothesis first emerged in the context of studies that investigated the role of behavioral stress in the development of experimental hypertension in laboratory animals. Those studies showed that regular exposure of animals to familar avoidance tasks evoked an anticipatory hypoventilatory breathing pattern associated with sustained increases in pCO₂. Repeated evocation of this breathing pattern potentiated the development of experimental hypertension when combined with high sodium intake. Subsequent studies of ambulatory monitoring of human breathing showed that people also engage in episodes of breathing inhibition in the natural environment. Experimental studies found that when hydrated humans voluntarily decreased breathing frequency and thereby increased pCO₂, they retained sodium and increased plasma volume. It was hypothesized that humans with high resting pCO₂ might show the same blood pressure sensitivity to high sodium intake as observed in the animal studies in which pCO₂ was increased via behavioral stress. This hypothesis was confirmed in two experimental studies, suggesting that high resting pCO₂ might be a useful clinical marker for sodium sensitivity. Recent studies have also found that older women with high resting end tidal CO₂ tend to have higher resting systolic blood pressure than other women with lower resting end tidal CO₂. Additional studies are needed to further clarify the role of breathing habits in pCO₂ regulation and its role in blood pressure adaptations to high sodium diet.