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I. Physiologisches Institut, Ruprecht-Karls-Universität Heidelberg, D-69120 Heidelberg, Germany
The aim of this study was to investigate the influence of the
mean level and phasic modulation of NO on the dynamic autoregulation of
renal blood flow (RBF). Transfer functions were calculated from
spontaneous fluctuations of RBF and arterial pressure (AP) in conscious
resting dogs for 2 h under control conditions, after NO synthase (NOS)
inhibition
[NG-nitro-L-arginine methyl
ester hydrochloride
(L-NAME)] and after L-NAME followed by a continuous
infusion of an NO donor
[S-nitroso-N-acetyl-DL-penicillamine (SNAP)]. After L-NAME
(n = 7) AP was elevated, heart rate
(HR) and RBF were reduced. The gain of the transfer function above 0.08 Hz was increased, compatible with enhanced resonance of the myogenic
response. A peak of high gain around 0.03 Hz, reflecting oscillations
of the tubuloglomerular feedback (TGF), was not affected. The gain
below 0.01 Hz, was elevated, but still less than 0 dB, indicating
diminished but not abolished autoregulation. After L-NAME and SNAP
(n = 5), mean AP and RBF were not
changed, but HR was slightly elevated. The gain above 0.08 Hz and the peak of high gain at 0.03 Hz were not affected. The gain
below 0.01 Hz was elevated, but smaller than 0 dB. It is concluded that
NO may help to prevent resonance of the myogenic response depending on
the mean level of NO. The feedback oscillations of the TGF are not
affected by NO. NO contributes to the autoregulation below 0.01 Hz due
to phasic modulation independent of its mean level.
renal hemodynamics; transfer function; tubuloglomerular feedback; myogenic response; nitric oxide donor
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