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These results suggest that acetylcholine-induced pulmonary vasorelaxation is mediated by two components: NO and a cytochrome P450 metabolite likely to be an EDHF. Propofol selectively attenuates acetylcholine-induced relaxation by inhibiting both of these endothelium-derived mediators.

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However, FSGS because of IFN-b is an exceedingly rare occurrence. On review of literature, 12 cases were encountered. Among them, 10 were Black, 8 female, 8 hypertensives, and 3 were obese. 2,6,[11][12][13][14] Also, 4 of the cases were patients with MS on interferon treatment. 2,6,11,13,15 Our case demonstrates some similarities to those reported as our patient was a woman. However, our patient was a White with a normal body mass index and not diagnosed with hypertension. Using the Naranjo criteria questionnaire for determining the likelihood of whether an adverse drug reaction is actually due to the drug, our patient scores a 6, implying it is probable. 16 Our patient was similar to 5 other reported cases where the symptoms resolved after stopping interferon, starting steroids, and immunomodulators. Moreover, they also had their renal function returned to baseline and complete laboratory remission. 2,[11][12][13] This case represents a rare adverse effect of INF-b in MS. Physicians should draw attention to symptoms and findings of nephropathy during IFN-b therapy, as routine work-up do not include renal function tests and urinalysis.