H₂S is well-known as hypotensive agent, whether it is synthetized endogenously or administered systemically. Moreover, the H₂S donor NaHS has been shown to inhibit vasopressor responses triggered by stimulation of preganglionic sympathetic fibers. In contradiction with this latter result, NaHS has been reported to facilitate transmission within sympathetic ganglia. To resolve this inconsistency, H₂S and NaHS were applied to primary cultures of dissociated sympathetic ganglia to reveal how this gasotransmitter might act at different subcellular compartments of such neurons. At the somatodendritic region of ganglionic neurons, NaHS raised the frequency, but not the amplitudes, of cholinergic miniature postsynaptic currents via a presynaptic site of action. In addition, the H₂S donor as well as H₂S itself caused membrane hyperpolarization and decreased action potential firing in response to current injection. Submillimolar NaHS concentrations did not affect currents through K_υ7 channels, but did evoke currents through K _ATP channels. Similarly to NaHS, the K _ATP channel activator diazoxide led to hyperpolarization and decreased membrane excitability; the effects of both, NaHS and diazoxide, were prevented by the K _ATP channel blocker tolbutamide. At postganglionic sympathetic nerve terminals, H₂S and NaHS enhanced noradrenaline release due to a direct action at the level of vesicle exocytosis. Taken together, H₂S may facilitate transmitter release within sympathetic ganglia and at sympatho-effector junctions, but causes hyperpolarization and reduced membrane excitability in ganglionic neurons. As this latter action was due to K _ATP channel gating, this channel family is hereby established as another previously unrecognized determinant in the function of sympathetic ganglia.

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