Increased vasoconstrictor sensitivity in obstructive sleep apnea

Abstract

We studied vasoconstrictor sensitivity and cholinergic responsiveness of the forearm vasculature in 10 male patients with obstructive sleep apnea (OSA) and 10 healthy controls. Subjects with regular medication, known arterial hypertension, diabetes mellitus, or dyslipidemia were not included in this study. Age, body mass index, blood pressure, blood glucose, serum lipids, and baseline forearm vascular conductance (derived from venous occlusion plethysmography and intra-arterial blood pressure measurement) did not differ significantly between these two groups. With use of three dosage steps each, angiotensin II and acetylcholine were successively infused into the brachial artery. During infusion of angiotensin II, mean conductance was 39.6% lower (P = 0.002) in the OSA patients compared with that in the control subjects. Vascular responsiveness to increasing dosages of acetylcholine was not significantly altered in the OSA group. These findings suggest an enhanced vasoconstrictor sensitivity in the forearm vasculature in OSA. The hypothesis that endothelial function in OSA is impaired independently of other cardiovascular risk factors is not supported by the present results.

Sleep Apnea and Cardiovascular Disease

“…81 However, other studies using correlative approaches in patients with comorbidities reported an inverse relationship between brachial artery flow-mediated dilation and sleep apnea severity. 104 Conflicting findings with regard to resistance vessel endothelial function in OSA 105,106 speak to the importance of careful exclusion of comorbidities in studies of OSA patients. Nevertheless, recent data suggest not only that conduit vessel endothelial function may be impaired in OSA but also that the impairment may be related to endothelial cell apoptosis and that treatment with CPAP may improve endothelial function.…”

14 nights of intermittent hypoxia elevate daytime blood pressure and sympathetic activity in healthy humans

“…Several studies have proposed impaired vasodilation as a likely contributor to high blood pressure in OSAS patients [13,36]. This work should be interpreted with caution, since many confounding factors (e.g.…”

Role of Endothelin in Intermittent Hypoxia-Induced Hypertension

“…It has been shown that chronic hypoxia decreases vascular sensitivity to vasoconstrictors, 33,34 so that elevated ET-1 levels under that setting may not stimulate increased systemic blood pressure. In contrast, sleep apnea has been associated with increased vasoconstrictor responses 6,35 and decreased vasodilator responses. 6 Therefore, increased vascular reactivity coupled with elevated circulating ET-1 may contribute to the pathogenesis of IH-induced hypertension.…”