Maxi-K+ Channel β1 Expression in Sleep Apnea Patients and Its Modulation by CPAP Treatment

BACKGROUND Maxi-K+ channels play a major vasodilator role in the regulation of arterial tone. Hypoxia clownregulates the expression of the maxi-K+ channel beta 1-subunit in rat and human arterial myocytes, thus facilitating vasoconstriction. We have investigated the relationships among hypoxemia, arterial pressure, and the expression of the beta 1-subunit in patients with severe obstructive sleep apnea-hypopnea syndrome (SAHS), a highly prevalent condition that predisposes to hypertension. METHODS We studied 20 male patients with strong clinical suspicion of SAHS. Overnight polysomnography and 24-h ambulatory blood pressure monitoring were performed in each patient. Evaluation of beta 1-subunit mRNA expression was made by a simple blood test using peripheral blood leukocytes (PBLs). The last two determinations were repeated 3 months after initiation of continuous positive airway pressure (CPAP) treatment. RESULTS In untreated obstructive SAHS patients, beta 1-subunit mRNA levels were correlated with the minimum level of overnight blood 02 saturation (r(2) = 0.56, P < 0.05) and systolic arterial pressure (r(2) = 0.64, P < 0.01). Notably, the correction of nocturnal hypoxemia with CPAP resulted in upregulation of beta 1-subunit mRNA and to a parallel significant decrease of systolic and diastolic arterial pressures of 6.5 and 5.3 mm Hg, respectively. CONCLUSIONS These observations, although preliminary, suggest that the maxi-K+ beta 1-subunit could contribute to vascular dysregulation in SAHS patients. Leukocyte beta 1 expression may be an independent readout of hypoxemia that could be useful as molecular marker for impending hypertension.