Fig. 14.

Proposed mechanisms of sulfide-induced contraction. Shown on the left and middle are the effects of applying (at the arrows) high (300–1,000 μM) and low (30 μM) Na₂S concentrations to the myograph solution chamber on the solution sulfide concentration (trace A), NAD(P)H autofluorescence (trace B), mitochondrial membrane potential (trace C), and tension development (trace D) observed in rat pulmonary arteries. The 2 phases of contraction, separated by the intervening relaxation to a tension nadir, are indicated. One the right, the events observed or proposed to occur during each of these 3 phases of the response to high concentrations of sulfide are shown, as are their proposed relationships to each other. The events following the application of a low concentration of sulfide are proposed to be similar to those occurring during Ph2 of the response to high sulfide concentrations: metabolism of sulfide by SQR leading to electron transport chain (ETC) stimulation, hyperpolarization of ΔΨ, ROS production by complex 3, and contraction. No nadir of contraction occurs with 30 μM Na₂S because the cellular sulfide concentration never gets high enough to block the ETC and therefore ROS production. In both high and low concentrations of sulfide, stimulation of PKC, likely caused by sulfide-induced thiol signaling, also enhances tension development throughout the response. CCOx, cytochrome-c oxidase.