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[] The upregulation of endothelial nitric oxide (NO) through increasing the expression of hepatic/plasma ET-1 from cholangiocytes and ET B receptors from ECs, and the upregulation of inducible NO synthase (iNOS)-mediated NO and heme oxygenase-1 (HO-1)-mediated carbon monoxide (CO) in pulmonary intravascular monocytes, are responsible for intrapulmonary vascular dilations

Vitiello et al., 2023)

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Therefore, the possibility that cannabinoid-based interventions could modify the molecular architecture underlying stress responsivity should be considered a hypothesis that warrants rigorous longitudinal and mechanistic investigation in human populations