14 DAY TRIAL // Erectile dysfunction (or impotence), connected with retrograde ejaculation and the loss of seminal emission, is a well-known effect of diabetes in men.
A new research at the University of Nebraska Medical Center, Omaha, investigated the molecular mechanism that induces erectile dysfunction in diabetes, a step that could lead to improved ways of treating ED.
Male rats treated with streptozotocin (STZ) to inflict diabetes exhibit sexual and behavioral symptoms similar to human diabetes.
The team looked at the brain's paraventricular nucleus (PVN), located in the hypothalamus, which is linked to many functions, including sexual physiology (included penile erection) and behavior but also at the levels of central nitric oxide (NO) within the PVN.
NO is an important neurotransmitter for normal penile erection. Penile erection installs in response to the administration of N-methyl-D-aspartic 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 team supposed that the stopped NMDA mediated responses in diabetes reflects a perturbed NO mechanism within the PVN.
The rats were kept in a light/dark cycle, with standard temperature and humidity levels. Rats that were not injected with STZ served as controls. The experiments started at four weeks after the rats were injected.
One experiment looked at the effect of L-NMMA on NMDA mediated behavioral responses in normal rats; the second measured behavioral responses to NMDA or sodium nitroprusside (SNP), an NO donor in both control and diabetic rats; the third watched the effect of diabetes on nNOS protein in the PVN; the fourth assessed NMDA mediated behavioral responses in diabetic rats after restoring the nNOS protein in the PVN employing viral gene transfer.
When L-NMMA was employed to block NO production in the PVN, NMDA mediated penile erectile responses were stopped. NMDA-induced erections were clearly decreased in diabetic rats compared with non-diabetic rats. The nNOS protein levels in the PVN were decreased in rats with diabetes and restoring nNOS protein within the PVN of diabetic rats could improve the impaired NMDA induced erectile responses.
Thus, the ED in diabetes seems to be induced by a selective defect in the NO mechanisms within the PVN, due to the loss of the synthetic enzyme for NO within the cells of the PVN. Reactivating the enzyme could highly improve the sex life of diabetic patients.