Acute Pressor Response to Psychosocial Stress Is Dependent on Endothelium‐Derived Endothelin‐1

Fox, Brandon; Becker, Bryan K.; Loria, Analia S.; Hyndman, Kelly A.; Jin, Chunhua; Clark, Hannah; Johns, Robin; Yanagisawa, Masashi; Pollock, David M.; Pollock, Jennifer S.

doi:10.1161/jaha.117.007863

Cited by 23 publications

(16 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ET‐1 is released in response to a number of stimuli including acute and chronic stress, 38 hyperosmolality, 39 high sodium intake 39 and hypoxia 40 . Obesity is a disease of chronic tissue hypoxia, 41 a known stimulus for ET‐1 production from endothelial cells through activation of hypoxia inducible factor alpha (HIF‐1α) 42 .…”

Section: Et‐1 In Obesity: Clinical Implicationsmentioning

confidence: 99%

Endothelin‐1 in the pathophysiology of obesity and insulin resistance

et al. 2020

View full text Add to dashboard Cite

The association between plasma endothelin-1 (ET-1) and obesity has been documented for decades, yet the contribution of ET-1 to risk factors associated with obesity is not fully understood. In 1994, one of first papers to document this association also noted a positive correlation between plasma insulin and ET-1, suggesting a potential contribution of ET-1 to the development of insulin resistance. Both endogenous receptors for ET-1, ET A and ET B are present in all insulin-sensitive tissues including adipose, liver and muscle, and ET-1 actions within these tissues suggest that ET-1 may be playing a role in the pathogenesis of insulin resistance. Further, antagonists for ET-1 receptors are clinically approved making these sites attractive therapeutic targets. This review focuses on known mechanisms through which ET-1 affects plasma lipid profiles and insulin signalling in these metabolically important tissues and also identifies gaps in our understanding of ET-1 in obesity-related pathophysiology.

show abstract

Section: Et‐1 In Obesity: Clinical Implicationsmentioning

confidence: 99%

Endothelin‐1 in the pathophysiology of obesity and insulin resistance

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Stress, whether acute or chronic, increases ET-1 production. For instance, air-jet stress and psychosocial stress in response to cage switching in rodents cause an acute increase in plasma ET-1 [17,18]. ET-1 is also thought to play a role in early life stressinduced changes in cardiovascular function in rodents [19].…”

Section: Discussionmentioning

confidence: 99%

Elevated plasma endothelin-1 is associated with reduced weight loss post vertical sleeve gastrectomy

Jenkins

Williams

Dungey

et al. 2019

Surgery for Obesity and Related Diseases

View full text Add to dashboard Cite

Current research supports that obesity and insulin resistance are positively correlated with plasma endothelin‐1 (ET‐1) levels; however, the mechanisms leading to this increase in ET‐1 are not fully understood. Similarly, while some physiological effects of ET‐1 have been characterized, the full complexity of this hormone has yet to be described in tissues outside of the vascular system. To date, one of the best treatments available for morbid obesity, cardiovascular disease, and metabolic syndrome is bariatric surgery to quickly reduce body fat and the factors associated with obesity‐related disease. We hypothesize that vertical sleeve gastrectomy (VSG) will reduce plasma ET‐1 levels. This was tested by measuring plasma ET‐1 levels from twelve obese patients before VSG, 6 weeks after, and 6 months after surgery. The results indicate that 6 weeks following VSG, plasma ET‐1 levels increased by 24%; however, after 6 months, there was a 27% decrease compared to baseline. Average weight loss in this cohort was 11.3±2.4 percent body weight after 6 weeks and 21.4±5.7 percent body weight after 6 months. Interestingly, we observed an inverse relationship between baseline plasma ET‐1 and percent body weight loss 3 months (R2=0.45, p<0.05) and 6 months (R2=0.49, p=0.01) post bariatric surgery. Our results indicate that VSG reduces plasma ET‐1 levels, a possible mechanism for improved metabolic risk in these patients. These data also suggest that ET‐1 may inhibit weight loss or serve as a predictor of weight loss following bariatric surgery. Support or Funding Information This work is supported by NHLBI grant R00 HL127178 to JSS. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

show abstract

“…Finally, both experimental and population-based studies demonstrated increased ET-1 levels following psychosocial stress exposure in healthy and diseased subjects (21,56,59,83,140). Endothelin-1 is a potent vasoconstrictor and an important mediator of CVD development following chronic upregulation of the acute stress response (214).…”

Section: Hpa Axis Hormones and Endothelial Dysfunctionmentioning

confidence: 99%

“…Endothelin-1 is a potent vasoconstrictor and an important mediator of CVD development following chronic upregulation of the acute stress response (214). Moreover, a study conducted in 2018 found that ET-1 contributes to the hypertensive response following acute stress exposure by binding to the endothelin-A receptor (59).…”

Section: Hpa Axis Hormones and Endothelial Dysfunctionmentioning

confidence: 99%

Chronic stress and endothelial dysfunction: mechanisms, experimental challenges, and the way ahead

Sher

Geddie

Olivier

et al. 2020

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Although chronic stress is an important risk factor for cardiovascular diseases (CVD) onset, the underlying mechanisms driving such pathophysiologic complications remain relatively unknown. Here, dysregulation of innate stress response systems and the effects of downstream mediators are strongly implicated, with the vascular endothelium emerging as a primary target of excessive glucocorticoid and catecholamine action. This review article therefore explores the development of stress-related endothelial dysfunction by focusing on the following: 1) assessing the phenomenon of stress and complexities surrounding this notion; 2) discussing mechanistic links between chronic stress and endothelial dysfunction; and 3) evaluating the utility of various preclinical models currently employed to study mechanisms underlying the onset of stress-mediated complications such as endothelial dysfunction. The data reveal that preclinical models play an important role in our efforts to gain an increased understanding of mechanisms underlying stress-mediated endothelial dysfunction. It is our understanding that this provides a good foundation going forward and we propose that further efforts should be made to a) more clearly define the concept of stress and b) standardize protocols of animal models with specific guidelines to better indicate the mental complications that are simulated.

show abstract

Acute Pressor Response to Psychosocial Stress Is Dependent on Endothelium‐Derived Endothelin‐1

Cited by 23 publications

References 67 publications

Endothelin‐1 in the pathophysiology of obesity and insulin resistance

Endothelin‐1 in the pathophysiology of obesity and insulin resistance

Elevated plasma endothelin-1 is associated with reduced weight loss post vertical sleeve gastrectomy

Chronic stress and endothelial dysfunction: mechanisms, experimental challenges, and the way ahead

Contact Info

Product

Resources

About