D5 Dopamine Receptor Decreases NADPH Oxidase Reactive Oxygen Species And Blood Pressure Via Heme Oxygenase-1

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We tested the hypothesis that the excessive BP and Blood Vitals increased ROS production in D5−/− mice may be attributable to decreased heme oxygenase-1 (HO-1) expression and exercise. A 24 h of administration of hemin, an HO-1 inducer, elevated HO-1 expression and HO activity (6.8- and 1.9-fold, BloodVitals respectively) and normalized the elevated ROS manufacturing and BP in D5−/− mice. Expression of HO-1 protein and HO activity have been increased (2.3- and 1.5-fold, respectively) in HEK cells that heterologously expressed human wild-kind D5R (HEK-hD5R), however not the empty vector-transfected HEK-293 cells. Fenoldopam (Fen), a D5R agonist, increased HO activity (3 h), BloodVitals HO-1 protein expression, HO-1 and D5R colocalization and co-immunoprecipitation in HEK-hD5R cells. Cellular NADPH oxidase exercise was decreased by 35% in HEK-hD5R that was abrogated with silencing of the heme oxygenase 1 gene (HMOX1). HMOX1 siRNA also impaired the ability of Fen to decrease NADPH oxidase activity in HEK-hD5R cells. In summary, BloodVitals the D5R positively regulates HO-1 by way of direct protein/protein interplay in the brief-time period and by growing HO-1 protein expression in the lengthy-term. The impaired D5R regulation of HO-1 and ROS manufacturing contributes to the pathogenesis of hypertension in D5−/− mice.



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