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1 Departments of Medicine and Physiology and Biophysics, Division of Nephrology, Mayo Clinic and Foundation, Rochester, Minnesota 55905, and 2 Department of Cardiac Surgery, University of Heidelberg, IM Neuenheimer Feld 110 Heidelberg 69115, Germany
The role of nitric oxide (NO) in the
regulation of the intrarenal microcirculation in streptozotocin
(STZ)-induced diabetes mellitus in rats is not clear. We examined renal
cortical and papillary hemodynamics in STZ rats and determined the
effects of systemic inhibition and stimulation of NO synthesis. Renal blood flow in cortical (QCC),
and inner medullary ascending
(QAV) and descending
(QDV) vasa recta capillaries was
measured by fluorescence videomicroscopy in STZ Munich-Wistar rats and
nondiabetic control rats. Ten days after STZ injection (80 mg/kg ip),
basal QCC and QDV were significantly greater in
STZ rats (n = 16) compared with control rats (n = 15). Infusion of
NG-monomethyl-L-arginine
(L-NMMA, 15 mg/kg bolus, 500 µg · min
1 · kg1
iv) decreased QCC (
41%),
QAV (38%), and
QDV (37%) in control rats
(n = 6) and to a significantly greater
magnitude than in STZ rats (n = 7),
QCC (14%),
QAV (20%), and
QDV (25%). Coinfusion of
L-arginine
(L-Arg, 1 mg · kg1 · min1
iv) with L-NMMA increased
QCC to a significantly greater
extent (P < 0.01) in control rats
compared with STZ rats. In subsequent studies, infusion of
L-Arg alone increased
QCC (+50%),
QAV (+16%), and
QDV (+11%) in control rats
(n = 5) but had no effect in STZ rats
(n = 5). These results show that the
response of renal cortical and papillary capillary blood flow to both
inhibition and stimulation of NO synthesis is attenuated in the early
onset of STZ-diabetes mellitus rats compared with control rats.
experimental insulin-dependent diabetes mellitus; nitric oxide-dependent renal vasodilation; diabetic endothelial dysfunction; NG-monomethyl-L-arginine; videomicroscopy
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