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Departments of Medicine and Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota 55905
We
investigated the role of prostaglandins in the renal vascular response
to exogenous and endogenous adenosine in control and streptozotocin
(STZ) diabetic rats. Exogenous adenosine (0.01-100 nmol) injected
into the abdominal aorta decreased renal blood flow (RBF) in a
dose-dependent manner to a much greater extent in STZ rats than in
control rats (P < 0.001). Inhibition
of prostaglandin synthesis with indomethacin (Indo; 10 mg/kg iv) potentiated the adenosine-induced renal vasoconstriction in
control rats but not in STZ rats. In control rats, Indo shifted the
dose response curve of exogenous adenosine-induced RBF reductions to
the left by a factor of 10 (ED50:
from 5.5 ± 0.51 to 0.55 ± 0.07 nmol adenosine, n = 6, P < 0.001) and in STZ rats only by a
factor of two (ED50: from 0.32 ± 0.03 to 0.16 ± 0.02 nmol adenosine,
n = 6, P > 0.05). The renal response to
endogenous adenosine was assessed by the magnitude of the postocclusive
reduction of RBF (POR), an adenosine-mediated phenomenon. POR was
greater in STZ rats (
65.3 ± 5.2%,
P < 0.001) compared with control
rats (36.2 ± 3.5%). Indo markedly enhanced POR in control
rats (20.3 ± 3.7%) but not in STZ rats (4.5 ± 2.7%). Renal cortical and medullary
PGE2 microdialysate concentrations and urinary PGE2 excretions were
clearly not lower in STZ (cortex: 169 ± 61 pg/ml; medulla: 640 ± 88 pg/ml, urine: 138 ± 25 pg/min) compared with
control rats (cortex: 99 ± 12 pg/ml; medulla: 489 ± 107 pg/ml;
urine: 82 ± 28 pg/min). Indo significantly decreased renal
cortical, medullary, and urinary excretion of
PGE2 in STZ and control rats.
These findings demonstrate that the adenosine-induced renal
vasoconstriction is increased in the presence of Indo in control rats
but not in STZ rats. The observations suggest that the diabetic renal
vasculature may have a diminished vasodilatory capacity in response to
prostaglandins to counteract adenosine-induced renal vasoconstriction.
renal hemodynamics; experimental insulin-dependent diabetes mellitus; indomethacin; diabetic dysfunctional vasoregulation; renal ischemia
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