Circulating anandamide and blood pressure in patients with obstructive sleep apnea

Engeli, Stefan; Blüher, Matthias; Jumpertz, Reiner; Wiesner, Tobias; Wirtz, H.; Bosse-Henck, A.; Stümvoll, Michael; Bátkai, Sándor; Pacher, Pál; Harvey-White, Judy; Kunos, George; Jordan, Jens

doi:10.1097/hjh.0b013e3283591595

Cited by 38 publications

(32 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To support this theory, several studies have shown positive correlations between circulating endocannabinoid levels and blood pressure. One study looking at potential correlations between circulating AEA and obstructive sleep apnea found that circulating AEA was a stronger determinant of blood pressure than sleep apnea severity, obesity, insulin resistance or inflammation (Engeli et al 2012). Another study in females with depression showed that diastolic and mean arterial blood pressures were positively correlated with serum levels of AEA and 2-AG ).…”

Section: Endocannabinoids and Hypertensionmentioning

confidence: 99%

“…Circulating levels of endocannabinoids are altered in a multitude of disorders including (but not limited to) obesity (Blüher et al 2006), diabetes and insulin resistance (Cote et al 2007;Abdulnour et al 2014), obstructive sleep apnea (Engeli et al 2012) and post-traumatic stress (Hauer et al 2013). In many studies, it has been shown that plasma levels of AEA and 2-AG are correlated with metabolic and cardiovascular risks (Weis et al 2010;Quercioli et al 2011), although it is not clear whether there is a causal link between these factors.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Endocannabinoids and the Cardiovascular System in Health and Disease

O’Sullivan

2015

Handbook of Experimental Pharmacology

View full text Add to dashboard Cite

The endocannabinoid system is widely distributed throughout the cardiovascular system. Endocannabinoids play a minimal role in the regulation of cardiovascular function in normal conditions, but are altered in most cardiovascular disorders. In shock, endocannabinoids released within blood mediate the associated hypotension through CB(1) activation. In hypertension, there is evidence for changes in the expression of CB(1), and CB(1) antagonism reduces blood pressure in obese hypertensive and diabetic patients. The endocannabinoid system is also upregulated in cardiac pathologies. This is likely to be cardioprotective, via CB(2) and CB(1) (lesser extent). In the vasculature, endocannabinoids cause vasorelaxation through activation of multiple target sites, inhibition of calcium channels, activation of potassium channels, NO production and the release of vasoactive substances. Changes in the expression or function of any of these pathways alter the vascular effect of endocannabinoids. Endocannabinoids have positive (CB(2)) and negative effects (CB(1)) on the progression of atherosclerosis. However, any negative effects of CB(1) may not be consequential, as chronic CB(1) antagonism in large scale human trials was not associated with significant reductions in atheroma. In neurovascular disorders such as stroke, endocannabinoids are upregulated and protective, involving activation of CB(1), CB(2), TRPV1 and PPARα. Although most of this evidence is from preclinical studies, it seems likely that cannabinoid-based therapies could be beneficial in a range of cardiovascular disorders.

show abstract

Section: Endocannabinoids and Hypertensionmentioning

confidence: 99%

mentioning

confidence: 99%

Endocannabinoids and the Cardiovascular System in Health and Disease

O’Sullivan

2015

Handbook of Experimental Pharmacology

View full text Add to dashboard Cite

show abstract

“…Endocannabinoid (eCB) signaling is critical for regulating arterial contractility in response to physiological and pathological stimuli (Engeli et al, 2012; Lípez-Miranda, Herradón, & Martín, 2008). The endocannabinoid system (eCBS) consists of eCB-producing enzymes, eCB ligands, eCB receptors (mostly CB1 and CB2 types), and the eCB degradation machinery (Lu & Mackie, 2016).…”

Section: Introductionmentioning

confidence: 99%

Maternal alcohol exposure during mid-pregnancy dilates fetal cerebral arteries via endocannabinoid receptors

Seleverstov

Tobiasz

Jackson

et al. 2017

Alcohol

View full text Add to dashboard Cite

Prenatal alcohol exposure often results in fetal alcohol syndrome and fetal alcohol spectrum disorders. Mechanisms of fetal brain damage by alcohol remain unclear. We used baboons (Papio spp.) to study alcohol-driven changes in the fetal cerebral artery endocannabinoid system. Pregnant baboons were subjected to binge alcohol exposure via gastric infusion three times during a period equivalent to the second trimester of human pregnancy. A control group was infused with orange-flavored drink that was isocaloric to the alcohol-containing solution. Cesarean sections were performed at a time equivalent to the end of the second trimester of human pregnancy. Fetal cerebral arteries were harvested and subjected to in vitro pressurization followed by pharmacological profiling. During each alcohol-infusion episode, maternal blood alcohol concentrations (BAC) reached 80 mg/dL, that is, equivalent to the BAC considered legal intoxication in humans. Circulating anandamide (AEA) and 2-arachidonoylglycerol (2-AG) remained unchanged. Ultrasound studies on pregnant mothers revealed that fetal alcohol exposure decreased peak systolic blood velocity in middle cerebral arteries when compared to pre-alcohol levels. Moreover, ethanol-induced dilation was observed in fetal cerebral arteries pressurized in vitro. This dilation was abolished by the mixture of AM251 and AM630, which block cannabinoid receptors 1 and 2, respectively. In the presence of AM251, the cannabinoid receptor agonist AEA evoked a higher, concentration-dependent dilation of cerebral arteries from alcohol-exposed fetuses. The difference in AEA-induced cerebral artery dilation vanished in the presence of AM630. CB1 and CB2 receptor mRNA and protein levels were similar in cerebral arteries from alcohol-exposed and control-exposed fetuses. In summary, alcohol exposure dilates fetal cerebral arteries via endocannabinoid receptors and results in an increased function of CB2.

show abstract

“…[33,49]). Thus, the plasma level of the endocannabinoid anandamide (AEA) is increased in hypertensive patients [8,21] and animals [21,45]. Moreover, the defective gene variant FAAH 129T of fatty acid amide hydrolase (FAAH; an enzyme responsible for AEA degradation) is associated with lower BP in young males [38].…”

Section: Introductionmentioning

confidence: 99%