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1 Division of Nephrology and Hypertension, Georgetown University Medical Center, Washington, District of Columbia 20007; 2 Second Department of Internal Medicine, University of Tokyo, Japan; and 3 Department of Physiology, Chonnam University Medical School, Kwangju, Korea
The spontaneously
hypertensive rat (SHR) has an enhanced tubuloglomerular
feedback (TGF) and a diminished buffering by juxtaglomerular apparatus
(JGA)-derived NO. We examined the hypothesis that these effects are due
to decreases in nitric oxide synthase (NOS) expression or limited
availability of L-arginine or
tetrahydrobiopterin (BH4). SHR
had significantly (P < 0.05) greater
mRNA abundance (by RT-PCR) or protein (by Western analysis) for
neuronal NOS (nNOS, or type I) and endothelial cell NOS (ecNOS, or type
III) in renal cortex or isolated glomeruli, respectively. There was
prominent expression of ecNOS in glomerular endothelium and nNOS in
macula densa. Maximal TGF responses, assessed from changes in proximal
stop-flow pressure during orthograde loop of Henle (LH) perfusion, were
greater in SHR [Wistar-Kyoto (WKY), 8.1 ± 0.3 (n = 46) vs. SHR, 10.3 ± 0.3 mmHg
(n = 57);
P < 0.001]. Unlike WKY, TGF
responses of SHR were unresponsive to microperfusion of the nNOS
inhibitor, 7-nitroindazole (7-NI,
10
4 M) [WKY, 9.5 ± 0.5 to 13.2 ± 0.7 (n = 13, P < 0.001) vs. SHR, 11.8 ± 0.7 to 12.5 ± 0.6 mmHg (n = 19, not
significant)], or to L-arginine
(103 M) [WKY, 7.7 ± 0.8 to 6.3 ± 0.4 (n = 10, P < 0.05) vs. SHR, 10.4 ± 0.7 to
10.6 ± 0.7 mmHg (n = 10, not
significant)]. Neither BH4 (104 M) nor sepiapterin
(104 M), its stable
precursor, modified TGF responses in WKY or in SHR, nor did they
restore a response to microperfusion of 7-NI in SHR. In conclusion,
there is a diminished role for NO from nNOS in blunting of TGF in SHR
which cannot be ascribed to limited NOS expression or availability of
substrate or BH4.
L-arginine; 7-nitroindazole; sepiapterin; tetrahydrobiopterin; nitric oxide; spontaneously hypertensive rat; juxtaglomerular apparatus
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