Center for Cardiovascular Diseases,
Houston, TX 77004
Tanzania
Research Article
The Role of Hypoxia-Inducible Factor/Prolyl Hydroxylation Pathway in Deoxycorticosterone Acetate/Salt Hypertension in the Rat
Author(s): Mohammad K Dallatu, Elizabeth Nwokocha, Ngozi AGU, Choi Myung, Mohammad A Newaz, Gabriela Garcia, Luan D Truong and Adebayo O OyekanMohammad K Dallatu, Elizabeth Nwokocha, Ngozi AGU, Choi Myung, Mohammad A Newaz, Gabriela Garcia, Luan D Truong and Adebayo O Oyekan
Kidney disease could result from hypertension and ischemia/hypoxia. Key mediators of cellular adaptation to hypoxia are oxygen-sensitive hypoxia inducible factor (HIF)s which are regulated by prolyl-4-hydroxylase domain (PHD)-containing dioxygenases. However, HIF activation can be protective as in ischemic death or promote renal fibrosis in chronic conditions. This study tested the hypothesis that increased HIF-1α consequent to reduced PHD expression contributes to the attendant hypertension and target organ damage in deoxycorticosterone acetate (DOCA)/ salt hypertension and that PHD inhibition ameliorates this effect. In rats made hypertensive by DOCA/salt treatment (DOCA 50 mg/kg s/c; 1% NaCl orally), PHD inhibition with dimethyl oxallyl glycine (DMOG) markedly attenuated hypertension (P<0.05), proteinuria (P<0.05) and attendant tubular interstitial changes and glomerula.. Read More»
Journal of Hypertension: Open Access received 614 citations as per Google Scholar report