Abstract
Currently, no treatment can completely cure pulmonary hypertension (PH), which can lead to right ventricular failure and, consequently, death. Therefore, searching for new therapies remains important. Increased resistance in pulmonary circulation is mainly caused by the excessive contraction and proliferation of small pulmonary arteries. Cannabinoids, a group of lipophilic compounds that all interact with cannabinoid receptors, exert a pulmonary vasodilatory effect through several different mechanisms, including mechanisms that depend on vascular endothelium and/or receptor-based mechanisms, and may also have anti-proliferative and anti-inflammatory properties. The vasodilatory effect is important in regulating pulmonary resistance, which can improve patients’ quality of life. Moreover, experimental studies on the effects of cannabidiol (plant-derived, non-psychoactive cannabinoid) in animal PH models have shown that cannabidiol reduces right ventricular systolic pressure and excessive remodelling and decreases pulmonary vascular hypertrophy and pulmonary vascular resistance. Due to the potentially beneficial effects of cannabinoids on pulmonary circulation and PH, in this work, we review whether cannabinoids can be used as an adjunctive therapy for PH. However, clinical trials are still needed to recommend the use of cannabinoids in the treatment of PH.
Highlights
Pulmonary hypertension (PH) refers to a group of clinical symptoms caused by increased blood pressure (BP) in the pulmonary circulation
Another objective of this review was to examine the evidence from experimental and human studies showing what endothelium-dependent mechanisms and/or receptors are involved in cannabinoid-mediated responses in the pulmonary vasculature, including cannabinoid receptors types 1 and 2 (CB1-Rs and CB2-Rs), historically called endothelial cannabinoid receptors, transient receptor potential vanilloids 1 and 4 (TRPV1 and TRPV4), peroxisome proliferator-activated receptors-γ (PPAR-γ), and prostanoid receptors
Cannabinoids are a group of lipophilic compounds that all interact with cannabinoid receptors (CB-Rs)
Summary
Pulmonary hypertension (PH) refers to a group of clinical symptoms caused by increased blood pressure (BP) in the pulmonary circulation. The aim of this review was to determine what vascular mechanisms are involved in cannabinoid-induced pulmonary vasodilation and what effects of cannabinoids have been observed to date during in vivo studies (including experimental PH) to produce a preliminary evaluation of the usefulness of cannabinoids in the assisted treatment of PH Another objective of this review was to examine the evidence from experimental and human studies showing what endothelium-dependent mechanisms and/or receptors are involved in cannabinoid-mediated responses in the pulmonary vasculature, including cannabinoid receptors types 1 and 2 (CB1-Rs and CB2-Rs), historically called endothelial cannabinoid receptors (eCB-Rs), transient receptor potential vanilloids 1 and 4 (TRPV1 and TRPV4), peroxisome proliferator-activated receptors-γ (PPAR-γ), and prostanoid receptors. This review only briefly describes the effects of cannabinoids on systemic vessels, as these effects have been discussed in detail in reviews by Stanley et al [14] and Bondarenko [15]
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