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Abstract 145: Knockout of Gamma-
 Adducin
 Impairs Vascular Function in Renal Arterioles in Association With Htn-Induced Renal Injury


 The FHH rat is a genetic model of hypertension that develops proteinuria, glomerulosclerosis, and chronic kidney disease. However, the genetic causes are unknown. We have previously identified an inactivating mutation of
 Add3
 in FHH rats in association with reduced
 ADD3
 expression and impaired myogenic reactivity of the renal arterioles. The vascular impairment and renal dysfunction were restored with knock-in of wild type (WT)
 Add3
 in FHH rats. The present study examined whether knockout (KO) of
 Add3
 in normal WT rats impairs the myogenic response of renal afferent arteriole (Af-art), interlobular arteriole (IA), arcuate arteriole (AA), renal blood flow (RBF) autoregulation, and if the reduction of expression of ADD3 promotes hypertension-induced renal dysfunction. Blood pressure was similar in 24-week old
 Add3
 KO vs. WT rats, and after induction of 3 weeks of DOCA-salt-hypertension in these strains. Proteinuria was significantly higher in both normotensive and hypertensive
 Add3
 KO compared with WT rats. KO of
 Add3
 abolished the myogenic response of Af-art compared with WT rats. Similarly, the diameters of IA and AA increased 46 % (from 55.28 ± 2.95 um to 80.39 ± 0.41 um) and 25 % (from 92.57 ± 9.51 um to 115.49 ± 11.68 um) respectively in
 Add3
 KO rats (n=4), while they remained unchanged in WT (n=5). Moreover, KO of
 Add3
 abolished the RBF autoregulation compared with WT rats. These results indicate that KO of
 Add3
 plays an important role to reduce the myogenic reactivity of renal arterioles and RBF autoregulation, and enhances renal damage after the onset of hypertension.
