Expression of Maxi-k+ Channel β1 Subunit in Peripheral Leukocytes, Blood Pressure Values and the Presence of Endothelial Dysfunction in Patients With Obstructive Sleep Apnea

Background: Several epidemiological studies have demonstrated that untreated OSA with continuous positive airway pressure, is related to high rates of cardiovascular morbidity and mortality, being HTA the most important cardiovascular morbidity associated with OSA. This relationship has been studied at three levels: clinical, subclinical and the basic research or molecular level. Most patients with OSA diagnosis have developed clinical hypertension and, because of the high prevalence of nocturnal hypertension in OSA, it would be essential to monitor blood pressure during sleep, using this device ambulatory blood pressure monitoring (ABPM). Regard to endothelial dysfunction, which can exist before irreversible vascular changes have occurred in the arterial wall (subclinical level) has been reported that patients with OSA have lower blood flow (measured by arterial flowmetry) and after treatment with CPAP, there is an improvement in endothelial function. At basic research level, in previous studies it has been observed that hypoxia down regulates the expression of Maxi-K+ Channel B1-subunit in smooth muscle cell and also in peripheral leukocytes. This channel is involved in the regulation of arterial vasodilation, being β1 subunit responsible for the vascular tone regulation. Basic research studies have shown the relationship between hypertension and ß1 subunit, describing that the expression of that unit decreases in hypertensive animal models. In a pilot study in OSA patients was suggested that ß1 subunit channel Maxi-K + could play an important role in vascular dysregulation of these patients. It has been also described a correlation between ß1 subunit level in vascular smooth muscle cells and its level in leukocytes.

Objective: To describe the relationship between OSA and hypertension from a clinical point of view (by performing ABPM), its relationship with endothelial dysfunction (by performing a flowmetry) and basic research level (by the determination of β1 subunit of the maxi-K channel +). This relationship between hypertension and OSA has been assessed at baseline condition in a group of OSA patients and a control group without OSA, and after changing the pathophysiological role of OSA treating with continuous positive pressure airway (CPAP) in the group of OSA patients.

Patients: Prospective study in which:

1. • We compared 61 patients with sleep apnea-hypopnea syndrome and 19 control subjects without OSA.
2. • In the group of 61 patients with OSA: we compared the results before and after three months of correct treatment with CPAP.

Measurements: