(Hypertension. 1996;27:377-381.)
© 1996 American Heart Association, Inc.
Articles |
Importance of Nitric Oxide and Prostaglandins in the Control of Rat Renal Papillary Blood Flow
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.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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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
pressure–renal blood flow relationship without altering
autoregulation. However, both nitric oxide and
prostaglandins importantly affected the renal perfusion
pressure–papillary blood flow relationship because L-NAME and
indomethacin significantly decreased this relationship
in an additive fashion. Although both drugs reduced the sensitivity of
the pressure–papillary 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
pressure–blood 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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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Nitric oxide and PGs are main controllers of renal function, and their effects include actions on renal hemodynamics and at the tubular level.1 2 3 At the present time, although the importance of these substances is widely recognized, the interaction between them in the control of kidney function is not completely established. Thus, in acute studies it has been suggested that in some circumstances, such as the administration of acetylcholine or bradykinin, both NO and PGs can compensate for the absence of each other to express their renal effects.3 4 5 6 However, except for some studies in rat models of renal failure,7 8 9 the role of these two vasodilator systems in the control of the renal microcirculation has not been directly evaluated in the normal animal.
Of special interest to the role of the kidney in hypertension is the renal medulla, especially the inner part or papilla. Interest in this area is maximal now, because it is thought that changes in PBF are important in the control of sodium excretion and of blood volume and pressure.10 11 The renal medulla has been shown to produce large amounts of PGs and NO that impair the kidney excretory function when inhibited.12 13 14 15 16 17 18 19 20 Moreover, selective pharmacological manipulation of the medullary circulation has been shown to affect blood pressure.21 22 Therefore, it is of great importance to gain insight into the mechanisms regulating the medullary microcirculation. In the present study, we have evaluated the role of NO and PGs in the acute control of rat PBF as well as their role in pressure-induced changes in blood flow.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Male Munich-Wistar rats born and raised in the Animalario of the Universidad de Murcia were used. In all experiments performed, the authors followed the guidelines of the European Union for the ethical treatment of animals.
Surgical Preparation
All experiments were performed in rats
fasted for 16 hours
before the experiment, following a method previously
described.18 23 The animals were anesthetized with
thiobutabarbital 100 mg/kg body wt IP (Inactin; Research Biochemical
International) and placed on a heated surgical table to maintain rectal
temperature at 36.5°C to 37°C. Catheters were inserted into the
right femoral artery to measure blood pressure and into the right
femoral vein for infusions. A tracheostomy tube was placed to
facilitate respiration. The left kidney was exposed by a midline
abdominal incision and placed in a holder specially built to isolate
the kidney from respiratory motion. Then, the renal papilla was exposed
by excising the ureter and was surrounded by moistened cotton. PBF was
measured with a laser Doppler flowmeter (Periflux PF3; Perimed).
The laser probe was fixed to a micromanipulator and placed on the
papillary surface at an angle of 
30°. RBF was determined by a
0.8-mm flow probe placed around the left renal artery connected to an
electromagnetic flowmeter (Skalar 1401, Skalar Medical). Zero flow was
obtained by carefully occluding the renal artery. In the autoregulation
experiments, an adjustable mechanical occluder was also placed around
the aorta, above the renal arteries, to allow for changes in RPP.
Finally, the abdominal opening was covered with a piece of Parafilm
(American National Can) to minimize evaporation. All animals received
an IV infusion of 0.9% NaCl solution containing 1% bovine serum
albumin at a rate of 1.5 mL/100 grams per hour. At least 60
minutes was allowed to elapse before the experiment was begun. MAP,
RBF, and PBF were continuously recorded throughout the experiment.
PBF was obtained as perfusion units and expressed as volts (100 U
corresponding to 1 V). The flowmeter was calibrated by using a
colloidal suspension of latex particles (Perimed motility standard),
which at room temperature gives a signal of 250 U (2.5 V, ±5%). At
the end of the experiment, the renal artery was completely occluded to
obtain a zero-flow reading in the laser Doppler flowmeter, and
this value (30 U, or 0.3 V), was subtracted from the signal
recorded during the experiment. Then, the rat was killed and the
left kidney was removed, blotted dry, and weighed.
Experimental Protocols
Protocol 1: Role of NO and PGs
in the Control of Renal
Papillary Circulation
In this series of experiments, a first group of
8 animals was
injected with L-NAME (10 mg/kg IV as a bolus, dissolved in 0.9%
saline; Sigma Chemical Co) and then with indomethacin
(7.5 mg/kg IV as a bolus, dissolved in 0.01 mol/L sodium carbonate;
Sigma Chemical Co). MAP, RBF, and PBF were measured immediately before
administration of the drugs (control) and when the
parameters became stable after the administration of each
drug, usually 10 to 15 minutes later. In the second group (n=6), the
order of administration of the drugs was reversed, with
indomethacin administered first and then L-NAME.
Protocol
2: Autoregulation Studies—Role of NO and
PGs
Autoregulation curves were obtained by determining RBF and PBF
at different RPP levels. This was done by tightening the aortic
occluder in 20 mm Hg steps, so that the kidney was perfused long enough
to record a stable flow value. As in protocol 1, two groups of
animals were studied. In the first group (n=9), these relationships
were obtained first in a basal situation, then after administration of
L-NAME (10 mg/kg IV bolus), and finally after administration of
indomethacin (7.5 mg/kg IV bolus). In the second group
(n=5), the order of administration of the drugs was reversed, and the
autoregulation curves were obtained in the basal state, then after
indomethacin, and finally after L-NAME.
Statistical Methods
Data are presented as mean±SEM.
Significance of the
differences in measured values within the groups was evaluated by use
of an ANOVA for repeated measures, followed by Duncan's
multiple-range test. The differences in measured values between
groups were analyzed by use of a two-way ANOVA followed by
Duncan's multiple-range test. Differences were considered
statistically significant at a level of P<.05.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Role of NO and PGs in the Control of Renal Papillary Circulation
In the first series of experiments, L-NAME significantly increased MAP from 114.8±3.9 to 145.7±3.2 mm Hg (a 27.8±3.6% increase) and decreased PBF from 2.18±0.09 to 1.31±0.07 V (a 39.4±3.8% decrease) and RBF from 6.9±1.1 to 3.7±0.6 mL·min-1·g-1 (a 47.4±1.9% decrease) (Fig 1
). The administration
of indomethacin in these animals did not significantly
change MAP (153.9±3.0 mm Hg) or RBF (3.4±0.9
mL·min-1·g-1)
but further decreased PBF by 35.2±2.5%, to 0.54±0.03 V. In this
group of animals, basal hematocrit was 0.46±0.008 and was well
maintained throughout the experiment.
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P<.05 between
groups. INDO indicates indomethacin; NAME, L-NAME.
In the second group, reversal of
the order of administration of drugs
produced essentially the same results (Fig 1
).
Indomethacin did not significantly change MAP (from a
basal level of 117.5±2.8 to 125.4±3.5 mm Hg) or RBF (from
6.4±1.0 to
6.3±0.9
mL·min-1·g-1)
but decreased PBF by 39.6±2.1% (from 2.13±0.09 to
1.28±0.04 V). The
subsequent injection of L-NAME also decreased PBF to 0.58±0.04 V (a
32.9±1.8% decrease) and RBF to 3.1±0.1
mL·min-1·g-1
(a 49.8±6.6% decrease) while it elevated MAP to 158.7±3.9 mm Hg
(a 28.3±2.5% increase). Basal hematocrit in this group was
0.45±0.007 and did not change throughout the experiment.
Autoregulation Studies: Role of NO and PGs
Fig
2 shows the results obtained in the group that
received first L-NAME and then indomethacin. In the
baseline period, the decrease in RPP from 120 to 100 mm Hg
significantly decreased PBF but did not alter RBF. Further decreases of
RPP lowered both RBF and PBF in a step-dependent manner.
Administration of L-NAME increased blood pressure and reduced both RBF
and PBF in a similar manner to that observed in protocol 1, but RBF and
PBF were autoregulated at 120 and 140 mm Hg, respectively. The
subsequent administration of indomethacin did not
statistically change the RPP-RBF or RPP-PBF relationships, but the
latter occurred at a much lower PBF because
indomethacin significantly decreased PBF.
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When the order of
administration of both drugs was reversed (Fig 3), indomethacin
did not alter the
RPP-RBF relationship but significantly altered that of PBF because of
the important PBF reduction that was elicited. However, similar to the
baseline period, PBF after indomethacin was not
autoregulated from 120 to 100 mm Hg. The subsequent administration of
L-NAME significantly decreased both RBF and PBF relationships in a
manner similar to that of the previous group, so that both flows were
autoregulated at pressures from 120 to 140 mm Hg. Basal hematocrit in
these two groups was 0.45±0.006 and 0.46±0.007, respectively,
and did
not change throughout the experiment.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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The results of the present study clearly indicate that both NO and PGs are major controllers of PBF in the normal rat. Inhibition of these two vasodilator systems reduced PBF
70% to 75% and converted
the blood pressure–sensitive papillary circulation into a bed with
a poor response to changes in blood pressure. Moreover, our experiments
also indicate that both NO and PGs contribute similarly to the
maintenance of normal PBF, and at least in these acute
experiments, a compensatory interaction between them is not supported
by the present data. Although the role of NO and PGs in the control of renal circulation has been extensively studied, the role of NO after PG synthesis inhibition or that of PG after NO inhibition has not been previously studied. Previous experiments4 5 6 suggested a compensatory role for these two compounds in the renal response produced after injection of endothelium-dependent vasodilators such as acetylcholine or bradykinin. Also, in endotoxemic rats, renal PG production was partly dependent on the elevated NO production.8 Our data, from experiments performed in anesthetized normal rats, do not support such an interaction between NO and PGs in the control of whole-kidney blood flow or in the papillary circulation. Contrary to the important role of PGs in the maintenance of renal perfusion in high-renin states,24 25 inhibition of PG synthesis in normal euvolemic animals does not decrease RBF,14 26 27 and this was also observed in the present data. In the present study, inhibition of NO synthesis greatly reduced RBF, indicating, as is widely recognized,3 the importance of NO in maintaining a normal renal perfusion. However, both the absolute and percent reductions in RBF induced by L-NAME were similar regardless of whether PGs were present. Inhibition of NO synthesis at the dose used in the present study should have maximally inhibited NO and then probably would have induced a compensatory elevation, if any, of vasodilatory PGs. The subsequent administration of indomethacin should have further decreased RBF. However, this was not the case, and RBF remained essentially unchanged with respect to the level observed after NO synthesis inhibition, therefore indicating the absence of a compensatory elevation of PGs after the acute blockade of NO. This reasoning, however, assumes that indomethacin inhibits only vasodilatory PGs; it is known that at the doses used, it also inhibits production of vasoconstrictor prostanoids, such as thromboxanes.27 Therefore, it is possible that an L-NAME–induced production of vasoconstrictor PGs could counteract the release of the vasodilatory PGs. In any case, these data confirm that NO plays a major role in the maintenance of RBF in the anesthetized normal rat.
In contrast to the effect of NO and PG inhibition observed at the whole-kidney level, a different effect was found in the papillary circulation. Our data show that both NO and PG synthesis inhibition affect the papillary circulation, and this agrees with previous reports by different groups. Inhibition of PGs either with indomethacin or meclofenamate has been shown to reduce vasa recta blood flow28 29 and PBF14 in the rat, and this effect is selective at the renal medullary level, as it has been shown that total RBF is not significantly affected. Similarly, NO synthesis inhibition also decreases vasa recta blood flow19 and reduces PBF in a dose-dependent manner.16 18 20 The present results extend these observations by showing that inhibition of PGs resulted in a similar decrease in PBF irrespective of the presence or absence of NO. The same can be said for NO synthesis inhibition. L-NAME decreased PBF in a similar amount in both the presence and absence of PGs. Overall, and contrary to what is observed at the whole-kidney level, these data clearly demonstrate that NO and PGs are the two major vasodilator substances that control, to a similar extent, an important percentage of PBF in the normal rat. However, similar to what was observed at the whole-kidney level, these data do not support a compensatory interaction between them.
In addition to their influence on basal vascular renal tone, both NO and PGs may modulate the responsiveness of renal vessels to several stimuli, among them pressure-induced vasodilation. Our results at the whole-kidney level with the L-NAME group completely agree with previous reports that found maintenance of blood flow autoregulation, albeit at a lower level, with inhibitors of NO synthesis in conscious and anesthetized dogs30 31 and in anesthetized rats.32 Moreover, they also show that combined blockade of NO and PGs does not further change the autoregulatory behavior observed after inhibiting only NO synthesis. Similar to what has been described above, inhibition of PGs did not modify the RPP-RBF relationship obtained either after or before L-NAME administration, again suggesting an apparent lack of involvement of PGs in this whole-kidney response.
In the renal papilla, the behavior is different and both inhibitors are able, by themselves, to reduce the relationship between RPP and PBF. However, it seems that only NO synthesis inhibition is able to maintain PBF at high RPPs. These results agree with previous studies20 that showed that low doses of L-NAME blunt the RPP-PBF relationship only at higher RPP levels. However, our experiments, performed with a larger dose of the NO synthesis inhibitor, show that L-NAME can clearly decrease the RPP-PBF relationship in a broader range of perfusion pressure levels, suggesting that NO is released not only at high perfusion pressures but also at low levels. This is similar to what is observed after indomethacin, which, as seen previously14 and in the present experiments, decreased the RPP-PBF relationship at a broad range of perfusion pressures. However, increasing RPP from 100 to 120 mm Hg significantly increased PBF. Therefore, these data indicate that both PGs and NO are important contributors to the pressure-induced vasodilation of the rat renal papillary circulation. However, our data suggest that NO is more important than PGs in maintaining the lack of autoregulation of the rat renal papillary circulation. The renal papillary circulation does not autoregulate as well as the cortex, and this has been demonstrated both in rats10 11 14 20 23 and in dogs.33 34 Several factors are thought to be involved in the lack of pressure-induced autoregulation of the renal papilla.10 11 Among them, the volume status of the animal seems to be an important determinant, since hydropenic rats demonstrate little change in PBF as renal perfusion pressure is increased.23 However, the present data, obtained in volume-expanded rats, clearly show that renal medullary blood flow is poorly autoregulated in the control periods, as previously described.23 The results of the present study also identify two major factors that affect the papillary pressure-flow relationship, NO and PGs.
In conclusion, the present results indicate that in the anesthetized rat, NO but not PGs contributes to the maintenance of total RBF without affecting its autoregulation. However, NO and PGs are the two major vasodilator systems that maintain the renal papillary perfusion. Inhibition of these two vasodilatory systems converts the pressure-sensitive papillary circulation into a bed very poorly responsive to changes in perfusion pressure.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported by grant No. 95/1717 from the Fondo de Investigaciones Sanitarias of the Ministerio de Sanidad y Consumo and grant No. SAF95-1549-C02-02 from the Comisión Interministerial de Ciencia y Tecnología de España.
Received August 16, 1995; first decision September 20, 1995; accepted November 21, 1995.
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