Adenosine-induced renal vasoconstriction in diabetes mellitus rats: role of prostaglandins

Renal cortex
DOI: 10.1152/ajpregu.1999.277.5.r1410 Publication Date: 2017-12-25T04:50:56Z
ABSTRACT
We investigated the role of prostaglandins in renal vascular response to exogenous and endogenous adenosine control streptozotocin (STZ) diabetic rats. Exogenous (0.01–100 nmol) injected into abdominal aorta decreased blood flow (RBF) a dose-dependent manner much greater extent STZ rats than ( P < 0.001). Inhibition prostaglandin synthesis with indomethacin (Indo; 10 mg/kg iv) potentiated adenosine-induced vasoconstriction but not In rats, Indo shifted dose curve RBF reductions left by factor (ED 50 : from 5.5 ± 0.51 0.55 0.07 nmol adenosine, n = 6, 0.001) only two 0.32 0.03 0.16 0.02 > 0.05). The was assessed magnitude postocclusive reduction (POR), an adenosine-mediated phenomenon. POR (−65.3 5.2%, compared (−36.2 3.5%). markedly enhanced (−20.3 3.7%) (−4.5 2.7%). Renal cortical medullary PGE 2 microdialysate concentrations urinary excretions were clearly lower (cortex: 169 61 pg/ml; medulla: 640 88 pg/ml, urine: 138 25 pg/min) 99 12 489 107 82 28 pg/min). significantly cortical, medullary, excretion These findings demonstrate that is increased presence observations suggest vasculature may have diminished vasodilatory capacity counteract vasoconstriction.
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