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pathologies, surgery, or injury can dismpt the autonomic pathways required for penile erection. Injury to the pelvic or cavemosus nerves can occur after abdominal perineal resection, radical cystectomy or rcdical pmstctcctomy. Furthermore, radiation to the pslvis for rectal, blcdder, or pmstcte malig. nancics can injure cavernous nsrses and result in motile dysftuwtion. Tmmurcthral resection of the prostate, extcmal sphincccr, or incision of urctbral strictures have Ixn repmtcd to CCUEC impotccm. However, the incidence atlerthese pr.xedures is Iesschan 10%. Imporenm may occur from thenncl injury to the cavamous nerves. Studies in expwicncncal animals has revealed that injury to the cavcmous nerves rmults in a loss of nitric oxide-containing fibers within WcpOrcal Cavcclmsus smowlt muscle. Denervation also triggers program CCIIdeatb-tmmwdapoptosis. ApptOsi~ Ofwrporeal ofsnwoth muscle results in repkm,nwctt witi ii. broustlssue that is unable to relax. Neurogsnic disordsm associaccd with intctruption of supraspinal, spinal or peripheral autonomic pathways may produce impotence. Spinal cord injury, multiple sciemsis, diabeccs, and P disease am commonly amociatcd with erectile dystiinction (20-90%). Autonomic neuropathies such as Olivo-Cembsllcr-Pontine dsgcnemcion or Shy Dragger’s disecsc result in impotence. Temporal Iobc epilspsy effcccing supraspinal centers hac alsa been associated with crcctile difficulties. Ercctile dystimction ofcanterorigin can occur from Icskofexcitction or inwcared inhibition of autonomic pathways, Evoked-potential testing offers no benefit over history and physical examination in diagnosis. Erectiie dystimction as the result of n+mmgenic causes presents unique opportunities as well as chalkngec with regard to therapy. Motor skills required to usc vcaum devices, implcncs, or imnuavernous injections may be impaired. H r i i jection or vasodilator such as pmstaglandin El we augmcnrad in patients with neumgenic causes, Ncwcc oml tlmmpisc such ac apomorphine acting within the brain or sildccmtl which a r ofncurogmic m t p m e s f impotcnc.e. K

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Wednesday,May13, BroadwayBallroomSouth, MOPM AngiotensinReceptorBlockadein the Treatment of CardiovascularDisease Effectsof ARB-ACEICombinationTherapyon MorbidityandMortalityin HeartFailure. Cohn JN,Universityof MinnesotaMedicalSchool, Minneapolis,Minnesota Angiotensinmayplaya pivotalrolein the SYC@OmS andprogressionof heartfailurebecause of itsvasoconstrictor, sodium-retamm “ “ g, tddosterone stimulating,andmyocardialandvascxdarsmooth musclegrowthpromotingeffects. Although angiotertsinconverting-enzyrn e (ACE)inhibitors wereintroducedas agentsto reducetheplasrnaand tissueconcentrationof sngiotensin,recentevidence suggeststhatangiotensinlevelspersistduring chronicACEinbibitortherapy. Thispersistence maybe relatedto non-sustainedsuppressionof ACE,increasedlevelsofangiotenainI, andhr alternatechymaaepathwaysfor conversionof angiotensirtIto angiotensinII. A pilotinvasive hemodynamicstudyhas demonstratedthat valsartan160mgbidaddedto conventiomd chroNc ACEinhibitortherapyfor 4 weeksproduces significantvasodijatorandhormonalinhibiting effects. lltereforeVal-HeFThaskeeninitiated (planned4300patientswithheartfailure)to explore the effectsof valsartsnaddedto all othertherapyon mortalityandmorbidity.

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