D5 Dopamine Receptor Decreases NADPH Oxidase Reactive Oxygen Species And Blood Pressure Through Heme Oxygenase-1: Difference between revisions

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Created page with "<br>We examined the speculation that the excessive BP and [https://git.koppa.pro/devinpye122650 BloodVitals home monitor] elevated ROS manufacturing in D5−/− mice could also be caused by decreased heme oxygenase-1 (HO-1) expression and exercise. A 24 h of administration of hemin, an HO-1 inducer, increased HO-1 expression and HO activity (6.8- and 1.9-fold, respectively) and normalized the elevated ROS production and BP in D5−/− mice. Expression of HO-1 protein..."
 
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Latest revision as of 13:17, 1 September 2025


We examined the speculation that the excessive BP and BloodVitals home monitor elevated ROS manufacturing in D5−/− mice could also be caused by decreased heme oxygenase-1 (HO-1) expression and exercise. A 24 h of administration of hemin, an HO-1 inducer, increased HO-1 expression and HO activity (6.8- and 1.9-fold, respectively) and normalized the elevated ROS production and BP in D5−/− mice. Expression of HO-1 protein and BloodVitals home monitor 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, elevated HO exercise (3 h), BloodVitals experience 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 additionally impaired the ability of Fen to lower NADPH oxidase activity in HEK-hD5R cells. In summary, the D5R positively regulates HO-1 by means of direct protein/protein interplay within the brief-term and by increasing HO-1 protein expression within the lengthy-time period. The impaired D5R regulation of HO-1 and ROS production contributes to the pathogenesis of hypertension in D5−/− mice.



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