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DTSTAMP:20130501T160000Z
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CATEGORIES:Conferences / Seminars / Lectures
DTSTART:20130501T160000Z
DTEND:20130501T170000Z
SUMMARY:Dissertation Defence - Loc Vinh Thang
DESCRIPTION:
 MACROPHAGE (MΦ)-DERIVED SUPEROXIDE DISRUPTS\n
 SYMPATHETIC 
 NERVE FUNCTION IN DEOXYCORTICOSTERONE\n
 ACETATE 
 (DOCA)-SALT HYPERTENSIVE RATS\n
 \n
 HOST: 
   JIM GALLIGAN\n
 \n
 More than 65 million 
 Americans have hypertension, which is a 
 major risk for stroke, heart and kidney disease. 
 Hypertension is a multi-organ disease that 
 involves changes in nervous and immune system 
 function. Sympathetic nerve activity is elevated 
 in some hypertensive humans and in some 
 animal models of hypertension, including the 
 Deoxycorticosterone acetate-salt (DOCA-salt) 
 model. DOCA-salt hypertension in rats is associated 
 with the impairment of a α2-adrenergic 
 autoreceptor (α2R), and increased 
 level of superoxide (O2-) and macrophage (M) 
 number in the mesenteric arterial 
 (MA) adventitia. However, the relationship between 
 M infiltration, O2- production 
 and α2R impairment are unknown. This dissertation 
 tested the hypothesis that as blood 
 pressure increases in DOCA-salt rats, M 
 infiltrate into the adventitia of MA. M 
 release O2- that disrupts α2R function 
 causing increased NE release and further 
 increases in blood pressure.  Time-course study 
 was used to determine the temporal relationship 
 between impaired function of sympathetic 
 nerve terminal α2R and adventitial infiltration 
 of pro-inflammatory M in 
 MA from DOCA-salt hypertensive rats. Liposomal-encapsulated 
 clodronate (LEC) was used to deplete 
 adventitial M. The results of 
 these studies revealed that pro-inflammatory 
 M infiltration and increased O2- level 
 in MA of DOCA-salt rats occurred after 10 days 
 of initial blood pressure increase, but α2R 
 impairment did not occur until a week 
 after the infiltration of M. Furthermore, 
 LEC prevented the development of the later 
 phases of DOCA-salt hypertension by blocked 
 the infiltration of M into the MA 
 adventitia, reduced O2- level in the MA, and 
 restored the α2R function. The novel aspect 
 of this study is that it tested the hypothesis 
 that M-derived O2- disrupts α2R 
 function, which further contributes to 
 the increase in blood pressure in DOCA-salt rats. 
 Hypertension is a major public health concern. 
 Therefore, clarifying the mechanism that 
 leads to enhanced neurogenic vasoconstriction 
 is important for new discoveries relevant 
 to anti-hypertensive drug development. Furthermore, 
 it is possible that vascular M 
 markers could be used in the future to identify 
 patients at risk for long-term changes in 
 sympathetic nerve function at the first diagnosis 
 of high blood pressure. \n\n
 Price: free\n
 Sponsor: Pharmacology & Toxicology\n
 Sponsor's Homepage: http://phmtox.msu.edu\n
 Contact name: Diane Hummel\n
 Contact phone: 884-3553\n
 Contact email: phm@msu.edu\n
LOCATION:B448-449 Life Sciences
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