Abstract P337: Angiotensin 1-7 Mitigates Oxidative Stress, Protects Renal Dopamine D1 Receptor Function and Prevents Development of Hypertension

• DOI: 10.1161/hyp.68.suppl_1.p337
• Publication Date: 2021-06-21T16:51:13Z
• Authors: Mustafa Lokhandwala; Andrea Diaz Diaz; Anees Ahamd Banday
• Keywords: Renal sodium reabsorption; Endothelial Dysfunction

The role of angiotensin in etiology cardiovascular diseases especially hypertension is well established. Renin-angiotensin-aldosterone contributes to the development and maintenance directly by increases vascular tone renal sodium reabsorption or indirectly increasing oxidative stress inflammation. Contrary this pathological arm, (Ang) 1-7 via Mas receptors has been reported protect function although exact mechanism not yet clear. We have previously shown that leads dopamine D1 receptor (D1R) dysfunction which could disrupt regulation subsequently lead hypertension. In here we wanted test whether chronic administration Ang mice mitigate stress, D1R prevent Mice (C57BL) were implanted with telemetry probes concomitantly treated L-buthionine sulfoximine (BSO, drinking water) (via jugular vein osmotic pumps). Control (C, no treatment) shams (implanted saline filled pumps) exhibited similar behavioral physiological parameters. BSO alone increased high BP as compared controls. treatment did affect control but prevented increase milieu mice. Mean arterial pressure (mmHg), C: 78.5 ± 2.3*; BSO: 97.3 3.8; 1-7: 80.1* 4.1; BSO+Ang 83.2 3.4*, *P <0.05 vs BSO. SKF38393, a agonist, urine excretion failed induce diuresis natriuresis BSO-treated Treatment protected both was observed plus 1-7. Chronic had effect on absence These data show disrupting dependent regulation. mitigates protects prevents BP. This study provides new insight how beneficial arm system D1R-mediated during stress.