Maxi-K+ Channel  1 Expression in Sleep Apnea Patients and Its Modulation by CPAP Treatment

• Published in: American journal of hypertension 2009-02, Vol.22 (2), p.197-202
• Main Authors: Navarro-Antolin, J., Carmona-Bernal, C., Rivero-Valdenebro, V., Villar, J., Capote, F., Lopez-Barneo, J.
• Format: Article
• Language: English
• Subjects: Continuous positive airway pressure
• ISSN: 0895-7061; 1941-7225
• DOI: 10.1038/ajh.2008.342

Maxi-K(+) channels play a major vasodilator role in the regulation of arterial tone. Hypoxia downregulates the expression of the maxi-K(+) channel beta1-subunit in rat and human arterial myocytes, thus facilitating vasoconstriction. We have investigated the relationships among hypoxemia, arterial pressure, and the expression of the beta1-subunit in patients with severe obstructive sleep apnea-hypopnea syndrome (SAHS), a highly prevalent condition that predisposes to hypertension. 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 beta1-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. In untreated obstructive SAHS patients, beta1-subunit mRNA levels were correlated with the minimum level of overnight blood O(2) 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 beta1-subunit mRNA and to a parallel significant decrease of systolic and diastolic arterial pressures of 6.5 and 5.3 mm Hg, respectively. These observations, although preliminary, suggest that the maxi-K(+) beta1-subunit could contribute to vascular dysregulation in SAHS patients. Leukocyte beta1 expression may be an independent readout of hypoxemia that could be useful as molecular marker for impending hypertension.