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Baek et al. reported that rocuronium bromide exerts differential regulatory effects on vascular endothelial cells, as demonstrated in cultured CPAE cells. Rocuronium bromide treatment suppressed endothelial nitric oxide synthase (eNOS) activity, leading to reduced nitric oxide (NO) production. Concurrently, the compound activated cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). This activation resulted in increased synthesis of prostaglandin E2 (PGE2).
Fig. 1 The effects of rocuronium bromide treatment on cyclooxygenase-1 (COX-1) in calf pulmonary artery endothelial (CPAE) cells. (Baek SB, et al., 2016)
References
Chompunud Na Ayudhya C, et al. demonstrated that rocuronium directly activates mast cell degranulation through distinct receptor pathways in mice and humans, providing the first evidence of MRGPRX2-mediated activation in human mast cells. In mouse peritoneal mast cells (PMCs), rocuronium (20 µg/mL) induced degranulation via MrgprB2, the murine ortholog of the human MRGPRX2 receptor. In human mast cells, degranulation required a higher concentration (≥500 µg/mL) and was mediated specifically through MRGPRX2. This study provides the first direct evidence that rocuronium induces degranulation in human mast cells through engagement of MRGPRX2.
Fig. 2 Rocuronium activates mouse peritoneal mast cells (PMCs) via MrgprB2. (Chompunud Na Ayudhya C, et al, 2021)
References
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