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Decreased aortal angiotensin converting enzyme 2 (ACE2) and phospho‐eNOS protein expression in db/db diabetic mice
Author(s) -
Kablan Narges M,
Chodavarapu Harshita,
Quan Rendong,
Difulvio Mauricio,
Elased Khalid M
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1088.4
Subject(s) - enos , medicine , endocrinology , angiotensin converting enzyme 2 , diabetes mellitus , renin–angiotensin system , nitric oxide synthase type iii , nitric oxide synthase , vasodilation , nitric oxide , pathogenesis , angiotensin ii , angiotensin converting enzyme , western blot , blood pressure , chemistry , biochemistry , disease , covid-19 , infectious disease (medical specialty) , gene
Cardiovascular disease is a long term complication of diabetes and remains a leading cause of morbidity and mortality. ACE2 is a homologue of ACE that preferentially converts the vasopressor angiotensin II (Ang II) to the vasodilator Ang (1–7). Endothelial nitric oxide synthase (eNOS) produces the endogenous vasodilator nitric oxide (NO). There is evidence that diabetes impairs ACE2 and NO‐mediated vasodilation. Our previous studies demonstrated an age‐dependent increase of blood pressure in db/db type 2 diabetic mice. The goal of this study was to investigate the role ACE2 and phospho‐eNOS in the pathogenesis of hypertension in db/db diabetic mice. Plasma and tissue ACE and ACE2 activities were measured. Western blot demonstrated a significant decrease in aortal ACE2 and phospho‐eNOS protein expression in 12 wk hypertensive db/db mice compared to controls (p<0.001). However, aortal renin, ACE, neprilysin and total eNOS protein expression were not altered in db/db mice. There was a significant increase in plasma ACE activity in db/db mice. In conclusion, down regulation of aortal ACE2 and phospho‐eNOS protein expression coupled with increased plasma ACE activity may contribute to the evolution of hypertension in db/db diabetic mice.