(Hypertension. 1995;26:1024-1029.)
© 1995 American Heart Association, Inc.
Articles |
From the Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson.
Abstract The purpose of this study was to determine the role
of nitric oxide in modulating the vasoconstrictor effect of
angiotensin II (Ang II) on renal segmental resistances in
the dog. To achieve this objective we examined the effect of intrarenal
infusions of Ang II on preglomerular and
postglomerular resistances in the presence and absence
of intrarenal nitric oxide synthesis inhibition established by an
intrarenal infusion of
NG-nitro-L-arginine-methyl
ester at 5 µg/kg per minute in dogs. The whole-kidney
stop-flow technique was used. Renal artery pressure was
servo-controlled at 78±2 mm Hg throughout the study. Intrarenal
infusion of Ang II alone at 0.5 and 2.0 ng/kg per minute increased
renal vascular resistance (
0.064±0.011 and
0.171±0.030
mm Hg/mL per minute, respectively) and decreased renal blood flow
(
21±4 and
45±9 mL/min). Associated with these changes,
glomerular hydrostatic pressure and
preglomerular resistance increased slightly
(
1.1±0.9 and
1.6±1.8 mm Hg;
0.008±0.005 and
0.030±0.010 mm Hg/mL per minute, respectively), and
postglomerular resistance increased markedly
(
0.046±0.011 and
0.116±0.026 mm Hg/mL per minute). When dogs
were pretreated with an intrarenal infusion of the nitric oxide
synthesis blocker, Ang II at 0.5 and 2.0 ng/kg per minute increased
renal vascular resistance (
0.271±0.058 and
1.088±0.242
mm Hg/mL per minute) and decreased renal blood flow (
28±5 and
62±9 mL/min). However, in sharp contrast to vehicle pretreatment,
Ang II decreased glomerular hydrostatic pressure
(
3.4±1.5 and
9.9±2.0 mm Hg), increased
postglomerular resistance (
0.122±0.029 and
0.439±0.133 mm Hg/mL per minute), and increased
preglomerular resistance (
0.109±0.031 and
0.487±0.099 mm Hg/mL per minute) in dogs pretreated with the
nitric oxide synthesis inhibitor. In summary, these data
indicate that during vehicle treatment Ang II infusion in the
stop-flow kidney had a predominant effect on
postglomerular resistance. However, when nitric oxide
synthesis was blocked, Ang II had a profound effect on
preglomerular resistance. These findings suggest that
nitric oxide may play an important role in protecting mainly
preglomerular vessels and to a lesser extent
postglomerular vessels from Ang IIinduced renal
vasoconstriction in dogs.
Key Words: nitric oxide angiotensin II dogs vasoconstriction kidney
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