Evidence that the nitrergic neurotransmitter and endothelium-derived relaxing factor might be S-nitrosothiols in the mouse corpus cavernosum.

The effects of thimerosal, a sulfhydryl oxidizing agent on nitrergic, endothelium-dependent and -independent relaxations were investigated to examine the possibility that the nitrergic neurotransmitter and endothelium-derived relaxing factor (EDRF) could be S-nitrosothiol or free nitric oxide (NO) in the isolated mouse corpus cavernosum. Thimerosal (5 x 10(-6)-2 x 10(-5) M) inhibited or almost abolished electrical field stimulation--(EFS, 30V, 0.5 ms, 15 sec, 1, 2, 4, 8, 16 Hz), acetylcholine--(ACh, 5 x 10(-8)-1.25 x 10(-6) M), glyceryl trinitrate--(GTN, 3 x 10(-7)-3 x 10(-6) M), and S-nitrosoglutathione--(GSNO, 5 x 10(-6)-1.25 x 10(-4) M) induced relaxations. Thiomerosal inhibition seems to be specific to L-arginine NO pathways since it had no effect on acidified sodium nitrite--(10(-4)-5 x 10(-4) M), photoactivated sodium nitrite--(2 x 10(-4) M), isoprenaline--(10(-6) M), or papaverine--(10(-4) M) elicited relaxations. Moreover, the inhibitory effect of thimerosal on the nitrergic, ACh- or GTN-induced relaxations were partly reversed by sulfhydryl-containing compounds, L-cysteine (10(-3) M), dithiothreitol (10(-3) M), or glutathione (10(-3) M). However L-methionine (10(-3) M), which contains a methyl group on the sulphur atom, failed to restore the thimerosal inhibition. Thimerosal did not change the contraction produced by 10(-4) M NG-nitro-L-arginine methyl ester. These findings indicate that the nitrergic neurotransmitter as well as EDRF may not be free NO but NO-transferring molecules, probably S-nitrosothiols, in the mouse corpus cavernosum.</p

Investigation the effect of propranolol, metoprolol and carvedilol on spermatogenesis in rat testis

Background: Coronary arterial diseases are one of the increasing disease around the worldwide. Because of common using of the beta blockers, we aimed to investigate the effect of different beta-adrenergic receptor blockers on spermatogenesis in male rats.Methods: Adult male Sprague Dawley rats were obtained. Totally 32 rats homogenized according to their weight and divided into four groups that each one includes eight rats. Three of groups were determined as drug groups and remained groups were determined as a control group. Propranolol 40mg/kg, Metoprolol succinate 60mg/kg, Carvedilol 30mg/kg dosage was given by oral gavage within the saline solution, and the only saline solution was given to control group for 21 days, respectively. After 21 days rats were sacrificed, and testis were extracted. Then, histopathologic evaluation was performed.Results: There was statistical significance both right and left testis volume of experimental between control and carvedilol groups (p<0.05). There was statistical histopathological significance between control and carvedilol (p<0.05), control and propranolol (p<0.05), metoprolol succinate and propranolol (p<0.05), metoprolol succinate and carvedilol groups (p<0.05), respectively.Conclusions: Beta-adrenergic receptor blockers have adverse effects on spermatogenesis. Especially propranolol and carvedilol that were non-selective, effects spermatogenesis worse than selective beta blockers such as metoprolol succinate. Extensive use of these drugs may affect spermatogenesis in male, so male patients who have a complaint of infertility should be questioned regarding the use of beta blockers

Investigation the effect of propranolol, metoprolol and carvedilol on spermatogenesis in rat testis

Background: Coronary arterial diseases are one of the increasing disease around the worldwide. Because of common using of the beta blockers, we aimed to investigate the effect of different beta-adrenergic receptor blockers on spermatogenesis in male rats.Methods: Adult male Sprague Dawley rats were obtained. Totally 32 rats homogenized according to their weight and divided into four groups that each one includes eight rats. Three of groups were determined as drug groups and remained groups were determined as a control group. Propranolol 40mg/kg, Metoprolol succinate 60mg/kg, Carvedilol 30mg/kg dosage was given by oral gavage within the saline solution, and the only saline solution was given to control group for 21 days, respectively. After 21 days rats were sacrificed, and testis were extracted. Then, histopathologic evaluation was performed.Results: There was statistical significance both right and left testis volume of experimental between control and carvedilol groups (p&lt;0.05). There was statistical histopathological significance between control and carvedilol (p&lt;0.05), control and propranolol (p&lt;0.05), metoprolol succinate and propranolol (p&lt;0.05), metoprolol succinate and carvedilol groups (p&lt;0.05), respectively.Conclusions: Beta-adrenergic receptor blockers have adverse effects on spermatogenesis. Especially propranolol and carvedilol that were non-selective, effects spermatogenesis worse than selective beta blockers such as metoprolol succinate. Extensive use of these drugs may affect spermatogenesis in male, so male patients who have a complaint of infertility should be questioned regarding the use of beta blockers