(Hypertension. 1996;27:377-381.)
© 1996 American Heart Association, Inc.
Articles |
From the Departamento de Fisiología, Facultad de Medicina de Murcia (M.C.O., N.M.A., T.Q., J.G.-E.), Madrid (V.L.), and Granada (F.V.), Spain.
Correspondence to Joaquín García-Estañ, Departamento Fisiología, Facultad de Medicina, 30100 Murcia, Spain. E-mail jgel@fcu.um.es.
Abstract The role of nitric oxide and
prostaglandins in the control of rat renal papillary blood
flow has been studied in anesthetized Munich-Wistar rats by use
of laser Doppler flowmeter. Acute administration of
N
-nitro-L-arginine methyl ester
(L-NAME) 10 mg/kg IV (n=8) increased mean arterial pressure
by 27.8±3.6%, decreased papillary blood flow by 39.4±3.8%, and
decreased renal blood flow by 47.4±1.9%. The subsequent
administration of indomethacin (7.5 mg/kg IV) further
decreased papillary blood flow (35.2±2.5%) without significant
changes in mean arterial pressure or renal blood flow. In a
second group (n=6), administration of indomethacin
before L-NAME decreased papillary blood flow by 39.6±2.1% without
significantly altering mean arterial pressure or renal
blood flow. The subsequent injection of L-NAME further decreased
papillary blood flow (32.9±1.8%) and renal blood flow
(49.8±6.6%)
while increasing mean arterial pressure to a level not
significantly different from that found in the first group.
Autoregulation studies showed that L-NAME but not
indomethacin reduced the renal perfusion
pressurerenal blood flow relationship without altering
autoregulation. However, both nitric oxide and
prostaglandins importantly affected the renal perfusion
pressurepapillary blood flow relationship because L-NAME and
indomethacin significantly decreased this relationship
in an additive fashion. Although both drugs reduced the sensitivity of
the pressurepapillary flow relationship, only L-NAME affected
autoregulation so that papillary blood flow was autoregulated at higher
renal perfusion pressures. Thus, the present results indicate that
both nitric oxide and prostaglandins control a similar
percentage of rat renal papillary blood flow, but nitric oxide seems to
be more important than prostaglandins as a mediator of the
pressureblood flow relationship. In contrast, only nitric oxide
modifies the renal blood flow level, although it does not disturb
whole-kidney blood flow autoregulation.
Key Words: kidney hypertension, arterial renal circulation homeostasis nitric oxide prostaglandins
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