AI Article Synopsis
- The study aimed to assess how sildenafil, which affects cyclic guanosine monophosphate (cGMP), influences contractions in the rat vas deferens and its relationship with the purinergic system.
- Experimental methods involved inducing contractions in isolated vas deferens samples using various substances like noradrenaline and ATP, while assessing the effects of sildenafil compared to other compounds like suramin and Evans blue.
- Results indicated that sildenafil inhibited contractions caused by electrical stimulation and ATP, suggesting that the purinergic system may play a significant role in this interaction, primarily via an ATP-dependent mechanism rather than direct receptor effects.
Article Abstract
Aim: To evaluate the effect of sildenafil, a selective inhibitor of cyclic guanosine monophosphate (cGMP)-selective type 5 phosphodiesterase, on isolated rat vas deferens and its connections with the purinergic system.
Methods: Epididymal and prostatic portions of isolated vas deferens were placed in organ baths containing Krebs' solution. Contractions were induced by noradrenaline (NA), adenosine triphosphate (ATP), alpha,beta-methylene ATP and electrical field stimulation (EFS). The effect of sildenafil on the contractions was compared with suramin and Evans blue (EB).
Results: NA, ATP, alpha,beta-methylene ATP and EFS caused contractions in both portions of vas deferens. NA-induced contractions were unaffected by sildenafil and suramin but potentiated by EB. ATP-induced contractions were non-competitively inhibited in both portions by sildenafil and suramin but potentiated by EB. alpha,beta-methylene ATP-induced contractions were unaffected by sildenafil but were inhibited in both portions by suramin and EB. EFS-induced contractions were inhibited by sildenafil and suramin while potentiated by EB.
Conclusion: Sildenafil inhibited the contractions in both portions of vas deferens, as did suramin. We have suggested that purinergic system has a role in this antagonism and it seems to be mediated by an ATP-dependent mechanism instead of a receptor interaction.
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| http://dx.doi.org/10.1111/j.1442-2042.2005.01127.x | DOI Listing |
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