Abstract withdrawn. (689.7)

Urinary Sodium Excretion Decreases In the Early Stages of Insulin Resistance In Model of Metabolic Syndrome Melissa E. Williams 1 , Jacqueline N. Minas 1 , Ruben Rodriguez 1 , Daisuke Nakano 2 , Akira Nishiyama 2 , and Rudy M. Ortiz 1 1 Department of Molecular & Cellular Biology, School of Natural Science, University of California Merced 2 Department of Pharmacology, Kagawa Medical University, Kagawa, Japan Type II diabetes is associated with abnormal activation of the renin‐angiotensin aldosterone system and impaired sodium (Na + ) regulation contributing to volume dependent hypertension. However, the mechanisms contributing to elevated systolic blood pressure (SBP) during the development of insulin resistance (IR) are not well defined. To examine the effects of the onset of IR to impaired U Na V and SBP, three groups of rats were studied for 6 weeks (n=6/group); 1) non‐IR, Long Evans Tokushima Otsuka (LETO), 2) untreated, IR Otsuka Long Evans Tokushima Fatty (OLETF), 3) OLETF + angiotensin receptor blocker (ARB; 10 mg olmesartan/kg/d for 3 weeks). Systolic blood pressure (SBP), urine Na + excretion (U Na V), and insulin resistance index (IRI) were measured at 9 and 15 weeks of age. At 9 weeks of age, the OLETF group exhibited a 43% increase in IRI compared to the LETO group. However, no differences in SBP and U Na V between LETO and OLETF were observed. At 15 weeks of age, the OLETFs experienced a 54% increase in IRI, accompanied by a 15% (145 mmHg) increase in mean SBP at 15 weeks, which was attributed to the 46% decrease in mean U Na V. This suggests that IR causes impaired renal Na + regulation, contributing to the onset of hypertension. Conversely, ARB treatment in OLETFs reduced SBP by 25% and increased U Na V by 50%, as well as a 24% decrease in IRI. This indicates that inappropriate activation of AT1 contributes to IR‐associated hypertension observed in OLETF.