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

AIM: Hydrogen sulfide (H2S) 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 H2S in the corpus cavernosum.

MAIN METHODS: Tension studies using isolated rat corpus cavernosum strips were conducted. Endogenous H2S 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 H2S. Blockade of CSE by BCA (10(-3)M) reduced the concentration of H2S 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 H2S 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 BaCl2 (3×10(-5)M) failed to reduce these relaxations significantly.

SIGNIFICANCE: H2S-induced relaxation of rat corpus cavernosum may be mediated - at least in part - through BKca and KV channels not by KATP and Kir channels. It also seems that K(+)-channels do not contribute to the synthesis of H2S.