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Abstract 52: Human Grk4{gamma}142v, Via Histone Deacetylase 1, Produces At1r-dependent Hypertension Oral Session VII: Concurrent A Clinical Issues
Human gene variants account for only a small proportion of essential hypertension in humans and have not been shown to produce hypertension in transgenic mice. The association between hypertension and 11 allelic variants of 8 candidate genes in humans (n=1074) was studied. We also evaluated the response to angiotensin receptor blockers (ARBs) in humans (n=681) and transgenic mice generated to express the human wild-type G protein-coupled receptor kinase 4 (hGRK4WT) or the 142V allele (hGRK4142V). hGRK4 variants (R65L, A142V, and A486V) were associated with essential hypertension; hGRK4142V, by itself, predicted the hyperte...
Source: Hypertension - October 30, 2013 Category: Cardiology Authors: Jose, P., Wang, Z., Sanada, H., Yoneda, M., Zheng, C., Williams, S., Bartlett, J., White, M., Gordon, L., Liu, M., Konkalmatt, P., Wang, X., Asico, L., Villar, V. A., Jones, J., Armando, I., Felder, R., Eisner, G. Tags: Oral Session VII: Concurrent A Clinical Issues Source Type: research

Abstract 75: Nrf2 Mediates the Antioxidant Effect of D2r Via Dj-1 in the Kidney Oral Session IX: Concurrent B Oxidative Stress
Renal dopamine D2 receptor (D2R) dysfunction is associated with increased oxidative stress and high blood pressure. We have reported that DJ-1 is regulated by D2R in the kidney. Nrf2 is a transcription factor that regulates the expression of several antioxidant genes. We hypothesize that Nrf2 is involved in the DJ-1-mediated regulation of reactive oxygen species (ROS) production in the kidney. DJ-1 and Nrf2 co-inmunoprecipitate in mouse kidney. Selective renal silencing of D2R in mice by the renal subcapsular infusion of D2R siRNA (~50%) decreases Nrf2 expression (63.4%±3.4, n=7, P<0.05), and silencing of D2R exp...
Source: Hypertension - October 30, 2013 Category: Cardiology Authors: Cuevas, S., Yang, Y., Assico, L., Feranil, J., Jones, J., Armando, I., Jose, P. A. Tags: Oral Session IX: Concurrent B Oxidative Stress Source Type: research