Sainz-Cort Alberto, Heeroma Joost H
GH Medical, Carrer d'Osca 4B, Sant Boi de Llobregat, Barcelona Spain.
GH Medical, Amsterdam, The Netherlands.
J Cannabis Res. 2020;2(1):23. doi: 10.1186/s42238-020-00030-4. Epub 2020 Jul 31.
Coronavirus disease 2019 (COVID-19) is spreading fast all around the world with more than fourteen millions of detected infected cases and more than 600.000 deaths by 20th July 2020. While scientist are working to find a vaccine, current epidemiological data shows that the most common comorbidities for patients with the worst prognosis, hypertension and diabetes, are often treated with angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs).
Both ACE inhibitors and ARBs induce overexpression of the angiotensin converting enzyme 2 (ACE-2) receptor, which has been identified as the main receptor used by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to enter into the alveolar cells of the lungs. While cannabinoids are known to reduce hypertension, the studies testing the hypotensive effects of cannabinoids never addressed their effects on ACE-2 receptors. However, some studies have linked the endocannabinoid system (ECS) with the renin angiotensin system (RAS), including a cross-modulation between the cannabinoid receptor 1 (CB1) and angiotensin II levels.
Since there are around 192 million people using cannabis worldwide, we believe that the mechanism underlying the hypotensive properties of cannabinoids should be urgently studied to understand if they can also lead to ACE-2 overexpression as other antihypertensive drugs do.
2019年冠状病毒病(COVID-19)正在全球迅速传播,截至2020年7月20日,已检测到超过1400万例感染病例,死亡人数超过60万。虽然科学家们正在努力寻找疫苗,但目前的流行病学数据显示,预后最差的患者最常见的合并症,即高血压和糖尿病,通常用血管紧张素转换酶(ACE)抑制剂和血管紧张素受体阻滞剂(ARB)治疗。
ACE抑制剂和ARB都会诱导血管紧张素转换酶2(ACE-2)受体的过度表达,该受体已被确定为严重急性呼吸综合征冠状病毒2(SARS-CoV-2)进入肺肺泡细胞所使用的主要受体。虽然已知大麻素可降低血压,但测试大麻素降压作用的研究从未涉及它们对ACE-2受体的影响。然而,一些研究将内源性大麻素系统(ECS)与肾素血管紧张素系统(RAS)联系起来,包括大麻素受体1(CB1)和血管紧张素II水平之间的交叉调节。
由于全球约有1.92亿人使用大麻,我们认为应紧急研究大麻素降压特性的潜在机制,以了解它们是否也会像其他降压药物一样导致ACE-2过度表达。