Intermittent hypoxia and arterial blood pressure control in humans: role of the peripheral vasculature and carotid baroreflex

Abstract

Intermittent hypoxia (IH) occurs in association with obstructive sleep apnea and likely contributes to the pathogenesis of hypertension. The purpose of this study was to examine the putative early adaptations at the level of the peripheral vasculature and carotid baroreflex (CBR) that may promote the development of hypertension. Ten healthy male participants (26 ± 1 yr, BMI = 24 ± 1 kg/m(2)) were exposed to 6 h of IH (1-min cycles of normoxia and hypoxia) and SHAM in a single-blinded, counterbalanced crossover study design. Ambulatory blood pressure was measured during each condition and the following night. Vascular strain of the carotid and femoral artery, a measure of localized arterial stiffness, and hemodynamic shear patterns in the brachial and femoral arteries were measured during each condition. Brachial artery reactive hyperemia flow-mediated vasodilation was assessed before and after each condition as a measure of endothelial function. CBR function and its control over leg vascular conductance (LVC) were measured after each condition with a variable-pressure neck chamber. Intermittent hypoxia 1) increased nighttime pulse pressure by 3.2 ± 1.3 mmHg, 2) altered femoral but not brachial artery hemodynamics, 3) did not affect brachial artery endothelial function, 4) reduced vascular strain in the carotid and possibly femoral artery, and 5) shifted CBR mean arterial pressure (MAP) to higher MAP while blunting LVC responses to CBR loading. These results suggest limb-specific vascular impairments, reduced vascular strain, and CBR resetting combined with blunted LVC responses are factors in the early pathogenesis of IH-induced development of hypertension.

Peripheral chemoreflex contribution to ventilatory long‐term facilitation induced by acute intermittent hypercapnic hypoxia in males and females

“…However, DBP and MAP did increase during the latter half of recovery following an air-breathing time-control and therefore, our conclusions are based on the first 30 min of recovery where IHH is the primary contributing factor. Lasting increases in blood pressure have been previously observed following both acute and chronic intermittent hypoxia in healthy individuals (Foster et al 2009;Gilmartin et al 2010;Tremblay et al 2016). Elevated blood pressure following IHH probably depends on sensory and sympathetic LTF through angiotensin-II type-I receptor signalling (Foster et al 2010;Jouett et al 2017).…”

Acute intermittent hypercapnic hypoxia and sympathetic neurovascular transduction in men

“…Following periods of IH, activation of the angiotensin-II type-I receptor (AT 1 R) (Fletcher et al 1999;Foster et al 2010;Marcus et al 2010;Jouett et al 2016) has been shown to contribute to the increased sympathetic vasomotor outflow and blood pressure observed in both healthy humans (Foster et al 2009(Foster et al , 2010Gilmartin et al 2010;Tremblay et al 2016;Jouett et al 2017) and animal models (Brooks et al 1997;Fletcher, 2000;Marcus et al 2009). This response depends on peripheral chemoreceptor afferent activity (Fletcher et al 1992) and afferent-efferent translation within brainstem centers, the median pre-optic nucleus and the subfornical organs (Saxena et al 2015;Shell et al 2019).…”

Impact of obstructive sleep apnoea and intermittent hypoxia on cardiovascular and cerebrovascular regulation

“…In a follow-up study using the same experimental IH model and a 14 day exposure, Tamisier et al (2011) found no change in calf reactive hyperaemia following a 5 min occlusion. Likewise, Tremblay et al (2016) found that 6 h of IH (ODI = 30) did not alter human brachial artery endothelial function assessed by flow-mediated dilatation. Consequently, prolonged IH exposure appears to be a prerequisite to induce endothelial dysfunction, whereas shorter duration IH may not impact or may even provide some beneficial effects to endothelial function, at least for the vascular beds examined in these studies.…”

“…Gilmartin et al (2010) found that 28 days of IH mimicking an ODI of 30 decreased forearm reactive hyperaemia in response to a 15 min ischaemic challenge (forearm occlusion), a response that is believed to be nitric oxide (i.e. Likewise, Tremblay et al (2016) found that 6 h of IH (ODI = 30) did not alter human brachial artery endothelial function assessed by flow-mediated dilatation. Unfortunately, as forearm reactive hyperaemia was not assessed after removal of IH, it is unclear how long this detriment persisted.…”