Identification of the vasodilatory endothelial cannabinoid receptor in the human pulmonary artery

Kozłowska, Hanna; Baranowska, Marta; Schlicker, Eberhard; Kozłowski, Mirosław; Laudański, J; Malinowska, Barbara

doi:10.1097/hjh.0b013e3282ef7a0a

Cited by 45 publications

(79 citation statements)

References 28 publications

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“…This receptor has been implicated in animal studies to be involved in mediating vasorelaxation to a range of cannabinoids in a variety of vascular beds, and is antagonised by an analogue of cannabidiol, O1918 [5], [26], [27], [28]. In agreement with these studies, we found that the effects of AEA in human mesenteric arteries were reduced by removal of the endothelium and in the presence of O-1918, further suggesting the existence of the proposed CB e receptor in humans [10], [23], [29]. The exact identity of this receptor is still unknown but a promising candidate is the orphan receptor GPR18.…”

Section: Discussionsupporting

confidence: 86%

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The endocannabinoid anandamide causes endothelium-dependent vasorelaxation in human mesenteric arteries

Stanley

Hind

Tufarelli

et al. 2016

Pharmacological Research

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Graphical abstractFAAH and COX1/2 do not modulate AEA-induced vasorelaxation. AEA induced-vasorelaxation is partially dependant on the CB1 receptor, the proposed CBe receptor, the endothelium and nitric oxide (NO). Analysis of AEA intracellular signalling suggests that AEA stimulates eNOS through MAPKs, AKT or Pi3K pathways. Dotted lines show potential linkage of signalling pathways. Fatty acid amide hydrolase (FAAH), cyclooxygenase-1 and -2 (COX1/2), anandamide (AEA), cannabinoid receptor (CB1), putative cannabinoid receptor (CBe), non-specific cannabinoid receptor (CBr), mitogen activated protein kinase family (MAPKs) phosphoinsitide 3-kinase (Pi3K), endothelial derived nitric oxide synthase (eNOS), nitric oxide (NO).

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Section: Discussionsupporting

confidence: 86%

“…In human pulmonary arteries, AEA also caused maximal vasorelaxation [23]. However, in the present study, both the potency and efficacy of AEA were lower.…”

Section: Discussioncontrasting

confidence: 72%

The endocannabinoid anandamide causes endothelium-dependent vasorelaxation in human mesenteric arteries

Stanley

Hind

Tufarelli

et al. 2016

Pharmacological Research

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“…However, in the same arteries, the vasorelaxant effect of 2-AG was not CB 1 mediated (Stanley and O'Sullivan 2014b). AEA and virodhamine-induced vasorelaxation of the human pulmonary artery is also not dependent on CB 1 (Kozlowska et al 2007;Kozlowska et al 2008;Baranowska-Kuczko et al 2014). …”

Section: Role For Cbmentioning

confidence: 79%

Endocannabinoids and the Cardiovascular System in Health and Disease

O’Sullivan

2015

Handbook of Experimental Pharmacology

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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.

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“…This is a finding common with a number of cannabinoid ligands in a range of vascular preparations [58,59] including human arteries [60]. To determine a potential role for calcium channels, some arteries were contracted using U46619 in calcium-free PSS, i.e.…”

Section: Discussionmentioning

confidence: 99%

Cyclooxygenase metabolism mediates vasorelaxation to 2-arachidonoylglycerol (2-AG) in human mesenteric arteries

Stanley

O’Sullivan

2014

Pharmacological Research

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Identification of the vasodilatory endothelial cannabinoid receptor in the human pulmonary artery

Cited by 45 publications

References 28 publications

The endocannabinoid anandamide causes endothelium-dependent vasorelaxation in human mesenteric arteries

The endocannabinoid anandamide causes endothelium-dependent vasorelaxation in human mesenteric arteries

Endocannabinoids and the Cardiovascular System in Health and Disease

Cyclooxygenase metabolism mediates vasorelaxation to 2-arachidonoylglycerol (2-AG) in human mesenteric arteries

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