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Angiotensin II (Ang II)‐induced oxidative stress stimulates adenosine release in the renal cortex
Author(s) -
Long L Stephen,
Zacharia Lefteris C,
Connors Stephanie,
Jackson Edwin K,
Welch William J
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.21.6.a1246-a
Adenosine, acting on type 1 receptors in the preglomerular vessels, reduces RBF. Since adenosine release is stimulated in the renal medulla during acute oxidative stress, we tested the hypothesis that chronic Ang II‐induced oxidative stress increases adenosine release in the renal cortex. We measured interstitial adenosine by intrarenal dialysis in the renal cortex and medulla of rats treated with vehicle (Veh, n=8) or Ang II (200 ng/kg/min, n=8) for 2 weeks, before and after injection of tempol (T, 72 mmol/kg). MAP was higher in Ang II rats (Ang II: 132±7 vs Veh: 102±6, p<0.001). Acute T normalized MAP in Ang II rats, but had no effect in Veh rats. Cortical dialysate adenosine was higher in Ang II rats (Ang II: 11.5±1.2 vs Veh: 6.1±1.2 pmol/μl, p<0.01), whereas medullary adenosine was not different (Ang II: 4.2±0.7 vs Veh: 3.5±1.0 pg/μl, ns). T reduced cortical adenosine levels in both groups (Ang II+ T: 6.2±0.5 pg/μl, p<0.05; Veh+ T: 2.6±0.4 pg/μl, p<0.01) and had no effect on medullary adenosine. Excretion of 8‐isoprostaglandin PGF2sub>α; (8‐iso) was higher in Ang II rats (Ang II: 27.5±1.3 vs Veh: 19.4±1.5 pg/min, p<0.05). T lowered 8‐iso excretion only in Ang II rats (Ang II + T: 14.2±2.1 pg/min, p<0.01). These results demonstrate that Ang II‐induced oxidative stress stimulates adenosine release in the renal cortex, suggesting that adenosine contributes to oxidative stress increases in RVR.