CPAP Therapy Delays Cardiovagal Reactivation and Decreases Arterial Renin-Angiotensin System Activity in Humans With Obstructive Sleep Apnea

Nicholl, David D M; Hanly, Patrick J.; Zalucky, Ann A; Mann, Michelle; MacRae, Jennifer M.; Poulin, Marc J.; Handley, George B.; Sola, Darlene Y.; Ahmed, Sofia B.

doi:10.5664/jcsm.7326

Cited by 11 publications

(6 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Blood pressure as study outcome measure was reported in ten RCTs totaling 407 participants [18][19][20][21][22][24][25][26][27][28]30 and ten PCS containing 297 participants 34,36,[39][40][41][45][46][47][48] (Table 2). CPAP treatment led to a blood pressure reduction.…”

Section: Resultsmentioning

confidence: 99%

Meta‐analysis of changes in the levels of catecholamines and blood pressure with continuous positive airway pressure therapy in obstructive sleep apnea

Green

Ken‐Dror

Fluck

et al. 2020

J of Clinical Hypertension

View full text Add to dashboard Cite

Obstructive sleep apnea (OSA) is a common condition among overweight and obese individuals. 1 About half of patients with OSA have hypertension, and about half of patients with hypertension have OSA. 2 Causal link between OSA and hypertension is complex and remains debatable, but hypertension may in part arise from increased sympathetic nerve activity induced by hypoxic stress. 3 OAS is associated with a number of secondary health complications, most notably cardiovascular disease, 4 and co-existing cardiometabolic risk factors such as dyslipidemia,

show abstract

Section: Resultsmentioning

confidence: 99%

Meta‐analysis of changes in the levels of catecholamines and blood pressure with continuous positive airway pressure therapy in obstructive sleep apnea

Green

Ken‐Dror

Fluck

et al. 2020

J of Clinical Hypertension

View full text Add to dashboard Cite

show abstract

“…Some studies indicated that continuous positive airway pressure (CPAP) treatment improves autonomic function assessed by HRV after eliminating physiological influences (e.g. arousal, hypoxia and respiratory events) in OSA population [51,52]. Thus, further investigations on the interplay between neuro-metaboliccardiac networking and OSA-related physiological alternations are needed.…”

Section: Impact Of Impaired Hrvmentioning

confidence: 99%

Heart rate variability during wakefulness as a marker of obstructive sleep apnea severity

Hua

Keenan

Mazzotti

et al. 2021

Sleep

View full text Add to dashboard Cite

Study Objectives Patients with obstructive sleep apnea (OSA) exhibit heterogeneous heart rate variability (HRV) during wakefulness and sleep. We investigated the influence of OSA severity on HRV parameters during wakefulness in a large international clinical sample. Methods 1247 subjects (426 without OSA and 821 patients with OSA) were enrolled from the Sleep Apnea Global Interdisciplinary Consortium. HRV parameters were calculated during a 5-minute wakefulness period with spontaneous breathing prior to the sleep study, using time-domain, frequency-domain and non-linear methods. Differences in HRV were evaluated among groups using analysis of covariance, controlling for relevant covariates. Results Patients with OSA showed significantly lower time-domain variations and less complexity of heartbeats compared to individuals without OSA. Those with severe OSA had remarkably reduced HRV compared to all other groups. Compared to non-OSA patients, those with severe OSA had lower HRV based on SDNN (adjusted mean: 37.4 vs. 46.2 ms; p<0.0001), RMSSD (21.5 vs. 27.9 ms; p<0.0001), ShanEn (1.83 vs. 2.01; p<0.0001), and Forbword (36.7 vs. 33.0; p=0.0006). While no differences were found in frequency-domain measures overall, among obese patients there was a shift to sympathetic dominance in severe OSA, with a higher LF/HF ratio compared to obese non-OSA patients (0.97 vs. 0.63; p=0.009). Conclusions Time-domain and non-linear HRV measures during wakefulness were associated with OSA severity, with severe patients having remarkably reduced and less complex HRV. Frequency-domain measures show a shift to sympathetic dominance only in obese OSA patients. Thus, HRV during wakefulness could provide additional information about cardiovascular physiology in OSA patients.

show abstract

“…Similarly, impaired vascular reactivity to different constrictor stimuli, such as Ang II and ET-1, has been reported in the aorta, as well as small mesenteric, cerebral and pulmonary arteries of CIH animal models ( 3 , 5 , 7 , 9 , 39 ). In individuals with OSA, arterial stiffness, as evaluated by the vasoconstrictor effects of intravenous Ang II challenge, was increased, which could be corrected by continuous positive airway pressure treatment ( 6 ). It was also found that the phosphorylation of p38 MAPK and ERK1/2 was increased by CIH, and the blockade of these kinases reduced Ang II-mediated contractions in both CIH aortic and mesenteric rings.…”

Section: Discussionmentioning

confidence: 99%

“…Obstructive sleep apnea (OSA) is a common disorder characterized by episodic arterial oxygen desaturation due to recurrent closure of the upper airway during sleep, namely intermittent hypoxia (IH), which can trigger excessive oxidative stress, systemic inflammation, sympathetic activation and increased renin generation, leading to abnormal vascular reactivity ( 1 , 2 ). IH-related vascular dysfunction involves impaired acetylcholine (ACh)-induced endothelium-dependent relaxation ( 3 , 4 ) and increased contractile responses to vasoconstrictors, such as angiotensin II (Ang II) ( 5 , 6 ) and endothelin-1 (ET-1) ( 7 – 9 ), which underlie the initiation and progression of hypertension. In our previous study, rats exposed to chronic IH (CIH) were found to exhibit enhanced Ang II-induced vasoconstriction, which was possibly attributed to the overactivation of ERK1/2 signaling through the upregulation of myosin phosphatase targeting subunit (MYPT1) and myosin light chain (MLC) phosphorylation ( 5 ).…”

Section: Introductionmentioning

confidence: 99%

O‑GlcNAcylation contributes to intermittent hypoxia‑associated vascular dysfunction via modulation of MAPKs but not CaMKII pathways

et al. 2021

View full text Add to dashboard Cite

Intermittent hypoxia (IH) leads to vascular dysfunction, and O-linked-β-N-acetylglucosamine (O-GlcNAc)ylation may regulate vascular reactivity through the modulation of intracellular signaling. The present study hypothesized that O-GlcNAc modifications contributed to the vascular effects of acute IH (AIH) and chronic IH (CIH) through the MAPK and Ca 2+ /calmodulin-dependent kinase II (CaMKII) pathways. Rat aortic and mesenteric segments were incubated with DMSO, O-GlcNAcase (OGA) or O-GlcNAc transferase (OGT) inhibitor under either normoxic or AIH conditions for 3 h, and arterial function was then assessed. Meanwhile, arteries isolated from control and CIH rats were exposed to 3 h of incubation under normoxic conditions using DMSO, OGA or OGT as an inhibitor, before assessing arterial reactivity. CIH was found to increase the expression of vascular O-GlcNAc protein and OGT, phosphorylate p38 MAPK and ERK1/2, and decrease OGA levels, but it had no effects on phosphorylated CaMKII levels. OGA inhibition increased global O-GlcNAcylation and the phosphorylation of p38 MAPK, ERK1/2 and CaMKII, whereas OGT blockade had the opposite effects. OGA inhibition preserved acetylcholine-induced relaxation in AIH arteries, whereas OGT blockade attenuated the relaxation responses of arteries under normoxic conditions or undergoing AIH treatments. However, the impairment of acetylcholine dilation in CIH mesenteric arteries was improved. CIH artery contraction was increased following angiotensin II (Ang II) exposure. Blockade of p38 MAPK and ERK1/2, but not CaMKII, attenuated Ang II-induced contractile responses in CIH arteries isolated from the non-OGT inhibitor-treated groups. OGT inhibition significantly blocked contractile responses to Ang II and abolished the inhibitory effects of MAPK inhibitors. These findings indicated that O-GlcNAcylation regulates IH-induced vascular dysfunction, at least partly by modulating MAPK, but not CaMKII, signaling pathways.

show abstract

CPAP Therapy Delays Cardiovagal Reactivation and Decreases Arterial Renin-Angiotensin System Activity in Humans With Obstructive Sleep Apnea

Abstract: CPAP therapy was associated with delayed cardiovagal reactivation after a stressor and down-regulation of the arterial RAS. These findings may have important implications in mitigating cardiovascular risk in both men and women with OSA.

Cited by 11 publications

References 53 publications

Meta‐analysis of changes in the levels of catecholamines and blood pressure with continuous positive airway pressure therapy in obstructive sleep apnea

Meta‐analysis of changes in the levels of catecholamines and blood pressure with continuous positive airway pressure therapy in obstructive sleep apnea

Heart rate variability during wakefulness as a marker of obstructive sleep apnea severity

O‑GlcNAcylation contributes to intermittent hypoxia‑associated vascular dysfunction via modulation of MAPKs but not CaMKII pathways

Contact Info

Product

Resources

About