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Erectile dysfunction in diabetes is due to selective defect in the brain

tic acid (NMDA) within the PVN. At the same time, inhibition of NO synthase with NG-monomethly-L-argining (L-NMMA) prevents NMDA-induced erection. The researchers hypothesized that the blunted NMDA mediated responses in diabetes reflects an impaired NO mechanism within the PVN. The involvement of an NO mechanism in the NMDA mediated behavioral response was also explored.

Methodology

The rats were exposed to a light/dark cycle, with standard temperature and humidity levels. The animals were randomly selected to receive chemical injection of the streptozotocin (STZ) to induce diabetes. Those rats that did not receive STZ (vehicle injected) served as controls. The experiments began on each of the rats four weeks after the injections.

Four experiments were conducted. Experiment one examined the effect of L-NMMA on NMDA mediated behavioral responses in normal rats; experiment two measured behavioral responses to NMDA or sodium nitroprusside (SNP), an NO donor in both control and diabetic rats; the third experiment observed the effect of diabetes on nNOS protein in the PVN; the fourth experiment measured NMDA mediated behavioral responses in diabetic rats after restoring the nNOS protein in the PVN using viral gene transfer.

Results

The researchers found that:

  • when L-NMMA was used to block NO production in the PVN, NMDA mediated penile erectile responses were blunted

  • NMDA-induced erections were significantly blunted in diabetic rats compared with control rats

  • the nNOS protein levels in the PVN were decreased in rats with diabetes and

  • restoring nNOS protein within the PVN of diabetic rats with viral gene transfer could alleviate the blunted NMDA induced erectile responses.

Conclusion

The researchers conclude that erectile dysfunction in diabetes is due to a selective defect in the NO mechanisms within the P
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Source:American Physiological Society


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