Abstract
To investigate the effect of hyperhomocysteinaemia (HHCy) on penile erectile function in a rat model, a methionine-rich diet was used in which erectile function, the reproductive system, and nitric oxide synthase were characterized. The intracavernous pressure, apomorphine experiments, measurement of oxidative stress, hematoxylin and eosin staining, immunohistochemistry analysis, reverse transcription-polymerase chain reactions and measurement of endothelial nitric oxide synthase activity were utilized. Our results showed that erections in the middle-dose, high-dose, and interference (INF) groups were significantly lower than the control (P < 0.05). INF group, being fed with vitamins B and folic acid, demonstrated markedly improved penile erections compared with the middle-dose group (P < 0.05). HHCy-induced eNOS and phospho-eNOS protein expression was reduced and the antioxidant effect was markedly impaired. The data of the present data provide evidence that HHCy is a vascular risk factor for erectile dysfunction by impairing cavernosa endothelial nitric oxide synthase activity. Intake of vitamins B can alleviate this abnormality.
Highlights
We found that the ratio of phospho-endothelial NOS (eNOS)-to-eNOS in the low, middle, and high-dose groups, and the INF group was significantly lower than the control group (P < 0.05)
Nitric oxide (NO), the key mediator synthesized by different NO synthase isoenzymes, plays an essential role in endothelial function[22,23,24]
Sexual stimuli induce an increase in serum levels of testosterone and the release of NO from penile nerve endings and endothelial cells, which in turn relax cavernous smooth muscle and increase blood flow to the penis[25]
Summary
A number of studies have shown that HHCy has a wide range of biological effects, such as damaging vascular endothelial cells, activating platelets, and stimulating vascular smooth muscle cell proliferation[12,13]. We speculated HHCy is caused by vascular endothelial damage, which might affect penile physiologic function. It is proposed that HHCy may affect activity and expression of nitric oxide synthase (NOS). Support for this hypothesis comes from the finding that HHCy inhibits acetylcholine-induced relaxation and cyclic guanosine monophosphate (cGMP) production in the rabbit corpus cavernosum in vitro[14]; the specific role of HHCy on ED is unclear.
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