The emergence of nitroxyl (HNO) as a biological signaling molecule is attracting increasing attention. HNO-based prodrugs show considerable potential in treating congestive heart failure, with HNO reacting rapidly with metal centers and protein-bound and free thiols. A new class of 2-(2-nitrophenyl)ethyl (2-NPE)-photocaged N-hydroxysulfonamides has been developed, and the mechanisms of photodecomposition have been investigated. Three photodecomposition pathways are observed: the desired concomitant C-O/N-S bond cleavage to generate HNO, sulfinate, and 2-nitrostyrene, C-O bond cleavage to give the parent sulfohydroxamic acid and 2-nitrostyrene, and O-N bond cleavage to release a sulfonamide and 2-nitrophenylacetaldehyde. Laser flash photolysis experiments provide support for a Norrish type II mechanism involving 1,5-hydrogen atom abstraction to generate an aci-nitro species. A mechanism is proposed in which the (Z)-aci-nitro intermediate undergoes either C-O bond cleavage to release RSO2NHO(H), concerted C-O/N-S bond cleavage to generate sulfinate and HNO, or isomerization to the (E)-isomer prior to O-N bond cleavage. The pKa of the N(H) of the N-hydroxysulfonamide plays a key role in determining whether C-O or concerted C-O/N-S bond cleavage occurs. Deprotonating this site favors the desired C-O/N-S bond cleavage at the expense of an increased level of undesired O-N bond cleavage. Triplet state quenchers have no effect on the observed photoproducts.