Potassium channels modulate the action but not the synthesis of hydrogen sulfide in rat corpus cavernosum

Abstract Aim Hydrogen sulfide (H 2 S) is a newly-introduced gasotransmitter in penile tissues. However, its exact mechanism of action in mediating penile erection is not fully elucidated. The major aim of this study was to examine the role of different K + channels in mediating the responses to H 2 S in the corpus cavernosum. Main methods Tension studies using isolated rat corpus cavernosum strips were conducted. Endogenous H 2 S production was measured using polarographic technique. Results are expressed as mean ± SEM. Key findings l -Cysteine (10 − 2  M) stimulated rat corpus cavernosum to produce H 2 S. Blockade of CSE by BCA (10 − 3  M) reduced the concentration of H 2 S produced from rat corpus cavernosum significantly. Addition of TEA (10 − 2  M) or 4-AP (10 − 3  M) didn't have a significant effect on the concentration of H 2 S produced. l -Cysteine (10 − 6 –10 − 2  M) elicited a concentration-dependent relaxation response which was significantly reduced by blockade of CSE using BCA (10 − 3  M). TEA (10 − 2  M), 4-AP (10 − 3  M) and TEA (10 − 4  M) attenuated l -cysteine-induced relaxation significantly. At 10 − 4  M, l -cysteine resulted in percentage relaxation of 1.55 ± 0.63, 10.94 ± 1.93 and 1.93 ± 0.80 in presence of TEA (10 − 2  M), 4-AP (10 − 3  M) and TEA (10 − 4  M) respectively compared to 23.78 ± 2.71 as control. Both glibenclamide (10 − 5  M) and BaCl 2 (3 × 10 − 5  M) failed to reduce these relaxations significantly. Significance H 2 S-induced relaxation of rat corpus cavernosum may be mediated - at least in part - through BK ca and K V channels not by K ATP and K ir channels. It also seems that K + -channels do not contribute to the synthesis of H 2 S.