Sleep deprivation and endothelial function: reconciling seminal evidence with recent perspectives

2021 ◽  
Vol 320 (1) ◽  
pp. H29-H35
Author(s):  
Joshua M. Cherubini ◽  
Jem L. Cheng ◽  
Jennifer S. Williams ◽  
Maureen J. MacDonald

Sleep is critical for the maintenance of physiological homeostasis and, as such, inadequate sleep beckons a myriad of pathologies. Sleep deprivation is a growing health concern in contemporary society since short sleep durations are associated with increased cardiovascular disease risk and atherosclerotic plaque development. Vascular endothelial dysfunction is an antecedent to atherosclerosis and cardiovascular disease. Herein, we review seminal literature indicating that short sleep durations attenuate endothelial function and explore more recent evidence indicating that sleep deprivation perturbs autonomic balance and the circadian rhythmicity of peripheral vascular clock components. We further examine literature that indicates a mechanistic link between short sleep duration and endothelial dysfunction and subsequent morbidity. Understanding the mechanisms that regulate endothelial function in the context of sleep deprivation facilitates the development and optimization of interventions, such as exercise, that mitigate the ramifications of inadequate sleep on vascular function and cardiovascular health. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/sleep-deprivation-and-endothelial-function/

2021 ◽  
Vol 13 (11) ◽  
pp. 5985
Author(s):  
Bryan Weichelt ◽  
Jeffrey VanWormer ◽  
Yin Xu ◽  
Chris Kadolph ◽  
Simon Lin

Cardiovascular disease (CVD) is a major public health concern in the United States. In response to the federally sponsored Million Hearts Risk Check Challenge, a team of programmers, software developers, health-information technologists, and clinicians in an integrated healthcare system in Wisconsin collaborated to develop Heart Health MobileTM (HHM), designed to improve awareness of cardiovascular disease risk and promote risk factor control among users. This paper outlines the development processes and highlights key lessons learned for mobile health applications. An agile project management methodology was used to dedicate adequate resources and employ adaptive planning and iterative development processes with a self-organized, cross-functional team. The initial HHM iOS app was developed and tested, and after additional modifications, gamified and HTML 5 versions of the app were released. The development of an iOS app is low in cost and sustainable by a healthcare system. Future app modifications to enhance data security and link self-reported cardiovascular risk assessment data to patient medical records may improve performance, patient relevance, and clinician acceptance of HHM in the primary-care setting. Legal and institutional barriers regarding the capture and analyses of protected health information must be mitigated to fully capture, analyze, and report patient health outcomes for future studies.


2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
J. Ruth Wu-Wong ◽  
William Noonan ◽  
Masaki Nakane ◽  
Kristin A. Brooks ◽  
Jason A. Segreti ◽  
...  

Endothelial dysfunction increases cardiovascular disease risk in chronic kidney disease (CKD). This study investigates whether VDR activation affects endothelial function in CKD. The 5/6 nephrectomized (NX) rats with experimental chronic renal insufficiency were treated with or without paricalcitol, a VDR activator. Thoracic aortic rings were precontracted with phenylephrine and then treated with acetylcholine or sodium nitroprusside. Uremia significantly affected aortic relaxation (% in NX rats versus % in SHAM at 30 M acetylcholine). The endothelial-dependent relaxation was improved to –%, –%, and –% in NX rats treated with paricalcitol at 0.021, 0.042, and 0.083 g/kg for two weeks, respectively, while paricalcitol at 0.042 g/kg did not affect blood pressure and heart rate. Parathyroid hormone (PTH) suppression alone did not improve endothelial function since cinacalcet suppressed PTH without affecting endothelial-dependent vasorelaxation. N-omega-nitro-L-arginine methyl ester completely abolished the effect of paricalcitol on improving endothelial function. These results demonstrate that VDR activation improves endothelial function in CKD.


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