Research Article: Relationship between the endothelial dysfunction and the expression of the β1-subunit of BK channels in a non-hypertensive sleep apnea group

Date Published: June 19, 2019

Publisher: Public Library of Science

Author(s): Candela Caballero-Eraso, Rocío Muñoz-Hernández, María Isabel Asensio Cruz, Rafael Moreno Luna, Carmen Carmona Bernal, Jose Luis López-Campos, Pablo Stiefel, Ángeles Sánchez Armengol, James Andrew Rowley.


Vascular damage must be diagnosed early in patients with hypertension. In this regard, endothelial dysfunction (ED) is an early sign of vascular disease and a predictor of cardiovascular diseases. In obstructive sleep apnea (OSA), intermittent hypoxia triggers ED, but mechanisms are not clear. In this context, it has been described that BK channels regulates arterial tone and that chronic and intermittent hypoxia downregulates the expression of the BK channel β1-subunit facilitating vasoconstriction. Thus, we investigated the relationship among hypoxemia, ED, and mRNA expression of the β1-subunit in patients with severe OSA. We aimed to assess (1) ED in non-hypertensive patients with OSA using laser-Doppler flowmetry, (2) BK β1-subunit mRNA expression, and (3) the impact of continuous positive airway pressure (CPAP) treatment on ED and β1-subunit regulation.

OSA patients underwent 24-hour blood pressure monitoring to exclude hypertension. Laser-Doppler flowmetry was performed to assess ED, and β1-subunit mRNA expression was evaluated using a blood test of peripheral blood leukocytes at baseline and after 3 months of CPAP treatment.

In normotensive patients with OSA, endothelial function correlated with the severity of OSA. CPAP improved endothelial function in normotensive OSA patients and the speed of the arterial response was significantly correlated with β1-subunit mRNA expression. β1-subunit mRNA expression at baseline correlated inversely with its change after CPAP.

Sleep apnea is related to ED in normotensive patients with OSA. CPAP therapy improves endothelial function and regulates β1-subunit mRNA expression.

Partial Text

The European Society of Hypertension and European Society of Cardiology (ESH/ESC) guidelines emphasize that subclinical vascular organ damage must be identified at an early, asymptomatic stage, because subclinical organ damage constitutes an intermediate stage in the continuum of vascular diseases such as hypertension. Similarly, early-stage organ damage is indicated by endothelial dysfunction (ED), which is currently considered one of the earliest signs of vascular disease and atherosclerosis, and it is a strong predictor of hypertension and other cardiovascular diseases [1–3].

We enrolled 21 patients (14 men, 7 women) with non-hypertensive, CPAP-naïve OSA. Table 1 shows the age, anthropometric parameters, and respiratory polygraphy results of the patients.

Cumulative evidence supports the clear relationship of OSA with cardiovascular disease (CVD). ED is an early clinical marker of atherosclerosis, and it has become a risk marker for development of cardiovascular disease and cardiovascular disease-related mortality [1,6,27]. Furthermore, it is an important cause of cardiovascular complications in OSA. Given the impact of untreated OSA on cardiovascular events [31–35], it is crucial to emphasize the role of CPAP in the risk of CVD, with a regulation of the ED. The present study aimed to analyze the role of CPAP in the ED and in the expression of the BK β1-subunit in a group of patients with OSA.




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