FOR IMMEDIATE RELEASE ON
MARCH 15, 2007
APS Contacts
Donna Krupa
Office:
(301) 634-7209
Cell: (703) 967-2751
dkrupa@the-aps.org
Erectile Dysfunction In
Diabetes Is Due To Selective Defect In The Brain
Defect
is result of a loss of synthetic enzyme, animal study finds
BETHESDA, MD A new study sheds additional
light on how erectile dysfunction (ED) interacts with diabetes. The study is
another step in uncovering the link between the two disorders, and may lead
to improved efficacy in treatments.
The study, Lack of Central Nitric Oxide Triggers
Erectile Dysfunction in Diabetes, was conducted by Hong Zheng, William G.
Mayhan, and Kaushik P. Patel, Departments of Cellular and Integrative
Physiology; and Keshore R. Bidasee, Department of Pharmacology, University
of Nebraska Medical Center, Omaha, NE. The results appear in the March 2007
edition of the American Journal of Physiology Regulatory,
Integrative and Comparative Physiology, one of 11 peer-reviewed
scientific publications issued monthly by The American Physiological Society
(APS) (www.The-APS.org).
Background
Sexual dysfunction is a well-recognized consequence of
diabetes mellitus in men. Erectile dysfunction, retrograde ejaculation and
the loss of seminal emission have all been described by such patients. This
study examined induced penile erection, yawning and stretch in diabetic
rats. Male Sprague-Dawley rats treated with streptozotocin (STZ) to induce
diabetes were used as they exhibit sexual and behavioral symptoms similar to
those found in diabetic men with sexual dysfunction.
The researchers focused on the paraventricular nucleus
(PVN) of the hypothalamus, located in the brain, an integration center
between the central and peripheral nervous systems. The site is involved in
numerous functions, including erectile function and sexual behavior, and is
a primary site within the forebrain that has been implicated in penile
erection. The investigators also examined central nitric oxide (NO within
the PVN) which plays an important role in the neurotransmission of normal
penile erection.
Penile erection is a behavioral response that occurs 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 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 PVN.
This defect is a loss in the synthetic enzyme for the production of NO
within the neurons of the PVN. Restoring this synthetic enzyme may have a
significant therapeutic value for diabetic patients with ED.
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JOURNAL PUBLICATION INFORMATION: American
Journal of Physiology Regulatory, Integrative and Comprehensive Physiology
March 2007.
NOTE TO EDITORS: To schedule an interview with a
member of the research team, please contact Donna Krupa at 301.634.7209
(office), 703.967.2751 (cell) or
DKrupa@the-APS.org.
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