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Department of Physiology, University of Alberta, Edmonton, Alberta, Canada T6G 2S2
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In the rat, the spleen is a major site of
fluid efflux out of the blood. By contrast, the mesenteric vasculature
serves as a blood reservoir. We proposed that the compliance and
myogenic responses of these vascular beds would reflect their different functional demands. Mesenteric and splenic arterioles (~150-200 µm) and venules (<250 µm) from rats anesthetized with
pentobarbital sodium were mounted in a pressurized myograph. Mesenteric
arterial diameter decreased from 146 ± 6 to 133 ± 6 µm on
raising intraluminal pressures from 80 to 120 mmHg. This response was
enhanced in the presence of
N
-nitro-L-arginine methyl ester
(L-NAME; 139 ± 6 to 112 ± 7 µm). There was no
such myogenic response in the splenic arterioles, except in the
presence of L-NAME (194 ± 4 to 164 ± 4.2 µm).
We propose that, whereas mesenteric arterioles exhibit myogenic
responses, this is normally masked by NO-mediated dilation in the
splenic vessels. The mesenteric venules were highly distensible
(active, 184 ± 15 to 320 ± 30.9 µm; passive in
Ca2+-free media, 209 ± 31 to 344 ± 27 µm;
4-8 mmHg) compared with the splenic vessels (active, 169 ± 11 to 184 ± 16 µm; passive, 187 ± 12 to 207 ± 17 µm). We conclude that, in response to an increase in perfusion
pressure, mesenteric arterial diameter would decrease to limit the
changes in flow and microvascular pressure. In addition, mesenteric
venous capacitance would increase. By contrast, splenic arterial
diameter would increase, while there would be little change in venous
diameter. This would enhance the increase in intrasplenic microvascular
pressure and increase fluid extravasation.
arteriole; venule; blood volume
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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WE HAVE DEMONSTRATED that the spleen contributes to the regulation of blood volume by controlling fluid extravasation from the intravascular space (1, 3, 7, 14, 16, 28). Fluid efflux is controlled hemodynamically. An increase in postcapillary relative to precapillary resistance leads to rise in capillary hydrostatic pressure and an increase in isoncotic fluid extravasation; there is no change in vascular permeability, the splenic vasculature being freely permeable to plasma proteins (16). Given that the rat spleen has no storage capacity and is bounded by a noncompliant capsule (23), the extravasate drains into the lymphatic system. We have shown in vitro and in vivo that nitric oxide (NO) and adrenomedullin cause differential vasoactivity of the pre-/postcapillary vessels of the spleen, such that microvascular pressure and fluid extravasation increase (1, 15). In response to both atrial natriuretic factor (ANF) and phenylephrine, there is pronounced constriction of the splenic veins (1, 27). It is unusual for veins to exhibit such a marked ability to constrict. However, unlike most veins, the splenic veins are endowed with a well-developed stratum of vascular smooth muscle (22).
Mesenteric arterioles are highly muscular and are capable of intense constriction. The mesenteric veins are less muscular, are highly distensible, and function as capacitance vessels (21). Such properties allow the mesentery to regulate blood flow to the small intestine and to act as a splanchnic reservoir (20). Differential reactivity to pharmacological agents has also been demonstrated in the rat mesentery; arteries demonstrate greater constriction than veins to norepinephrine, 5-hydroxytryptamine (5-HT), and vasopressin, whereas veins are more sensitive to the vasodilator effects of isoprenaline (32), i.e., just the opposite behavior to that seen in the splenic vasculature.
The myogenic response, an intrinsic property of vascular smooth muscle to constrict in response to an increase in intravascular pressure, is commonly observed in small arterioles (4, 19, 29, 30). These responses involve influx of Ca2+ via voltage-gated L-type Ca2+ channels (30) and are abolished by the removal of extracellular Ca2+ (29). A comparison of the responses in media with and without Ca2+ thus gives a measure of intrinsic myogenic or vascular tone.
Myogenic responses to an increase in intraluminal pressure have been reported in the rabbit facial vein (10, 18). Weak responses have also been reported in rat skeletal muscle and bat wing venules (5, 8). In the mesentery, only passive venous responses and compliance have been studied (11). The portal vein, into which the splenic veins flow, does however exhibit strong spontaneous myogenic contraction of longitudinal vascular smooth muscle (13, 24). We proposed therefore that the splenic vein would also exhibit high vascular tone.
Recently, it has been proposed that NO might act to modulate myogenic
reactivity (4). Small mesenteric arteries (~200 µm) in
endothelial NO synthase (eNOS) knockout mice exhibit stronger myogenic
responses than wild types (25), and in rat skeletal muscle
arteries, inhibition of NO biosynthesis with
N-nitro-L-arginine increases the
myogenic response. We wished to determine whether NO was
capable of modulating myogenic responses in mesenteric and splenic
arteries and veins by using
N-nitro-L-arginine methyl ester
(L-NAME) to inhibit NO synthase (NOS).
We used the pressurized myograph system to investigate the myogenic response to increases in intraluminal pressure in isolated mesenteric and splenic arteries and veins. Passive responses were studied in Ca2+-free media. A comparison of active and passive yielded a measure of vascular tone. The myogenic response was defined as a decrease in vessel diameter elicited by an increase in intraluminal pressure from 60 to 140 mmHg. We also measured wall thickness and determined the wall-to-lumen ratio, this being an important structural determinant of vascular reactivity; a larger wall-to-lumen ratio is indicative of greater constriction for a given degree of smooth muscle shortening (12, 26). Comparing splenic vessels with those in the mesentery allowed us to determine possible differential vascular functions of these vascular beds. We hypothesized that the myogenic responses of vessels from the spleen would be consistent with its ability to control blood volume by increasing capillary hydrostatic pressure, i.e., that in response to an increase in intraluminal pressure, there would be a myogenic response (decrease in vessel diameter) in the venules but not in the arterioles. By contrast, we proposed that the myogenic responses and distensibility of the mesenteric vessels would be consistent with that organ's role in controlling total peripheral resistance and splanchnic blood pooling, i.e., that in response to an increase in intraluminal pressure, there would be a myogenic response in the arterioles but that the venules would be highly distensible.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Experiments were examined by a local Animal Welfare Committee in agreement with the Canada Council on Animal Care. These experiments also comply with the American Physiological Society's "Guiding Principles for Research Involving Animals and Human Beings."
Animals and Housing
Male Long Evans rats (n = 47) were obtained from Charles River, St. Foy, Quebec, Canada. They were held in the animal facility for at least 1 wk before experimentation. Animals were exposed to a 12:12-h light-dark cycle in a humidity- and temperature-controlled environment while allowed access to water and 0.3% sodium diet ad libitum.Drugs and Solutions
Dulbecco's medium. DMEM base powder (8.3 g/l DMEM D5030, Sigma-Aldrich: no glucose, L-glutamine, phenol red, sodium bicarbonate, or sodium pyruvate) was added to 1 liter of pure water (DNase- and RNase free), 1 mM sodium pyruvate, 25 mM sodium bicarbonate, 5 mM HEPES (all from GIBCO Life Technologies), and 5 mM D-(+)-glucose (Sigma-Aldrich).
Ca2+-free Dulbecco's medium. DMEM base powder containing 15 mM HEPES and 15 mM glucose (14.8 g/l, Sigma-Aldrich: no L-glutamine, no sodium pyruvate, no phenol red, and also no calcium chloride) was added to 1 liter of pure water (DNase and RNase free), 1 mM sodium pyruvate, 25 mM sodium bicarbonate (all from GIBCO Life Technologies), and 1 µM EGTA (Sigma-Aldrich) as a chelating agent. All solutions were prepared in sterile conditions using sterile equipment and filtered using a vacuum pressure filtration system (0.22 µM Steri-cap filter, Millipore).
Surgical Procedures
Rats (250-400 g) were anesthetized with pentobarbital sodium (MTC Pharmaceuticals, 50 mg/kg ip) to enable removal of tissue, after which animals were given a lethal dose of Euthanol (Bimeda-MTC, 1 ml/kg) into the myocardium.Mesenteric vessels (n = 16). A segment (~10 cm) of the small intestine and attached mesentery ~20 cm in a retrograde direction from the ileal-cecal junction (proximal ileum) were removed through a midline laparotomy. The ileum was ligated at both ends, and the superior mesenteric artery and vein were cut so that the ileum and adjoining mesentery could be removed.
The mesentery was pinned to the Silastic bottom of the Petri dish containing cold (0-4°C) Dulbecco's medium with 1 g/l albumin (IgG and endotoxin free, Sigma-Aldrich) at pH 7.35-7.4. The mesenteric artery was cannulated (35-gauge Microfibril tubing, World Precision Instruments) and flushed with cold Dulbecco's medium (2 ml over 10 min) to remove blood and metabolites. Fourth-order arterioles (<200 µm at 80 mmHg, n = 8) or venules (<250 µm at 4 mmHg, n = 8) ~2 mm in length were isolated from the mesentery. (We have defined the order of vessel branching on the basis of the mesenteric/splenic artery being zero order. According to this classification, fourth-order vessels adjoin the ileum/splenic hilum at their distal end.) One vessel only was removed from each animal. All surgical instruments were autoclaved before use.Splenic vessels (n = 28). Through a midline laparotomy, the spleen and adipose tissue were dissected out. Blood was flushed out with cold Dulbecco's (10 ml) through the splenic artery over a 15-min period (~0.7 ml/min); we ensured that this was no greater than the physiological flow rate we have previously measured in the splenic artery (2.3 ± 0.4 ml/min; Ref. 15) so as to prevent endothelial damage. Fourth-order arterioles (<200 µm at 80 mmHg, n = 20) and venules (<250 µm at 4 mmHg, n = 8) were isolated from the spleen. One vessel only was removed from each animal.
Pressure Myograph
Without exposure to air, vessels were carefully transferred to the vessel chamber of the pressurized myograph and gradually allowed to warm to room temperature. The proximal inflow pipette was connected with Tygon tubing (2.4 mm OD × 0.8 mm ID) to a pressure servo system (PS200/Q, Living Systems Instrumentation).The vessel was mounted on the inflow pipette (tip diameter 100-125 µm for the arterioles, 180-200 µm for the venules) and secured with a sterile single fiber of a multifilament braided nylon thread. The proximal stopcock was then opened, and a gentle flow was allowed through the lumen of the vessel, keeping pressure <10 mmHg in arterioles and <2 mmHg in venules. Flow was stopped and the distal end of the vessel was mounted and tied onto the outflow pipette. The distal stopcock was then closed so that blind-sac (no-flow) experiments could be performed. Intraluminal pressure was then increased (100 mmHg, arterioles; 5 mmHg, venules), and it was ensured that no leak occurred, i.e., pressure could be maintained at these pressures without further flow into the vessel. The vessel chamber was slowly warmed to 37°C over 10-15 min and maintained at 37 ± 0.5°C throughout the duration of the experiment (Living Systems Instrumentation).
Vessels were viewed with a black and white CCD camera (Hitachi, Canada) and displayed on a monitor (Ultrak). Internal vessel diameter (ID) and wall thickness were measured using a video dimension analyzer (Living Systems Instrumentation). Both ID and intraluminal pressures were recorded for later off-line computerized analysis using WINDAQ (DATAQ Instruments).
Experimental Protocol
Vessels were both perfused and superfused (200 ml/h, ~2 bath changes/min) with Dulbecco's medium from a reservoir, maintained at 37°C, and bubbled with 95% air-5% CO2 (Praxair). Vessels were first allowed to stabilize for 30 min at a physiological flow rate (20 µl/min arterioles, 2 µl/min venules) to remove metabolites and then for 60 min at a physiological pressure (60 mmHg, arterioles; 4 mmHg, venules). Pressure was increased and monitored using the Pressure Servo Unit (Living Systems) attached to a calibrated pressure transducer at the inflow stopcock.Experiment 1: controls. Pressure was increased in stepwise increments from 20 to 140 mmHg in the arterioles (20 mmHg every 5 min) and from 2 to 12 mmHg in the venules (2 mmHg every 10 min). Preliminary studies revealed that vessel damage occurred at higher intraluminal pressures.
Experiment 2: L-NAME. Experiments were either repeated in the presence of L-NAME (100 µM) or its inactive enantiomer D-NAME (Sigma-Aldrich) added to the superfusate to inhibit NOS and allowed to stabilize for 30 min at 60 mmHg. At the end of the pressure steps, 1 µM acetylcholine chloride (Sigma-Aldrich) was added to the vessel chamber to confirm that NO was inhibited, i.e., that the vessel did not dilate.
Experiment 3: Ca2+ free. Experiments were repeated after the medium had been changed to Ca2+-free Dulbecco's, and allowed to stabilize for 30 min, to obtain the passive diameter of each vessel at each pressure step.
Experiment 4: S-nitroso-N-acetylpenicillamine. A further group of experiments were performed in splenic arterioles whereby experiment 2 was repeated and in the presence of the NO donor S-nitroso-N-acetylpenicillamine (SNAP) (30 µM) (Sigma-Aldrich).
In all experiments, vessels were tested for leaks at the end of the study to ensure that vessel integrity had been maintained throughout the experiment. For the purposes of this study, responses that occurred in Ca2+-free media will be referred to as the passive response, whereas changes in diameter occurring in Dulbecco's media will be termed the active response. The difference between the active and the passive response will be described as "vascular tone." The term "myogenic response" will be used to describe the constriction of a vessel in response to increases in intraluminal pressure. We chose as our reference point that pressure at which maximal diameter was observed, i.e., 60 mmHg for the mesenteric arteries and 80 mmHg for the splenic arteries. These pressures were estimated to be at the lower end of the in vivo intraluminal pressure of the vessels. Fenger-Gron et al. (9) have shown that, in the mesenteric vascular arcade, intraluminal pressure falls from ~115 mmHg in the superior mesenteric artery to ~75 mmHg in 100 µM vessels at the base of the mesenteric arcade (9). Preliminary experiments revealed that the intraluminal pressure in the splenic artery was also ~115 mmHg (unpublished observation). Given that the splenic vessels were of the same order as the mesenteric arterioles (at the base of the mesenteric arcade), we estimated that the normal in vivo pressures in these vascular beds also would be very similar. Wall-to-lumen ratio (h/R) was calculated from measurement of total wall thickness/external diameter at 100 mmHg for the arterioles, and at 6 mmHg for the venules, these being the intraluminal pressures at which vessels exhibited tone but were not overstretched (26).Statistical Analysis
Vessel diameters at each pressure step were compared with that measured at 60 mmHg (arterioles) or 4 mmHg (venules) using one-way ANOVA to determine within-group variation. Active (control) diameters were compared with active (L-NAME) and passive (Ca2+ free) diameters using two-way ANOVA for repeated measures, followed by Student-Neuman-Keuls post hoc test for multiple comparisons. Differences between h/R in mesenteric and splenic arterioles and venules were compared using a Student's paired t-test. The level of statistical significance was set at P < 0.05, with data being expressed as means ± SE.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Active vs. Passive Responses
Arterioles.
In response to stepwise increases in intraluminal pressure (80-140
mmHg), mesenteric arterioles (<200 µm at 80 mmHg) demonstrated myogenic responses (active) above 60 mmHg (Fig.
1A, 
). In splenic hilar
arterioles (<200 µm at 80 mmHg), no such responses were observed
(Fig. 1B, ). With increasing intraluminal pressure, there
was a steady increase in vascular tone (active minus passive) in the
mesenteric arterioles but not in the splenic arterioles (Fig.
2A).
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Venules.
Neither mesenteric nor splenic venules (<250 µm at 4 mmHg) exhibited
myogenic responses, i.e., vessel diameter did not decrease in response
to an increase in intraluminal pressure (Fig.
3, A and B, ).
Although both active and passive diameters of mesenteric venules
increased as intraluminal pressure rose (Fig. 3A), the distensibility and compliance of the splenic venules was markedly less
than that of the mesenteric venules (Fig. 3B). Both
mesenteric and splenic venules exhibited vascular tone [Fig. 3; 2-way
ANOVA, active diameters vs. passive diameters; P < 0.05].
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Effect of L-NAME
Arterioles.
After NOS inhibition with L-NAME, increased myogenic
responses were observed in small arterioles from both the mesentery and the spleen (Fig. 1, A and B, 
), i.e., in the
spleen, there was pressure-induced constriction in the previously
unresponsive arterioles. There was no significant difference between
the magnitude of the myogenic responses (decrease in diameter from the
maximum response) of mesenteric (solid line) and splenic arterioles
(broken line; Fig. 1D). By contrast, there was no such
myogenic response in splenic arterioles treated with D-NAME
[at 120 mmHg, vessel diameters were 189.6 ± 19.5 µm
(D-NAME, n = 5) vs. 191.0 ± 18.9 µm
(control, n = 5)]. In the presence of
L-NAME, both mesenteric and splenic arterioles exhibited
vascular tone, there being a significant increase in the difference
between the active and passive responses after an increase in
intraluminal pressure (Fig. 2A).
Venules. In mesenteric and splenic venules, active diameters tended to be lower in the presence of L-NAME (Fig. 3, A and B).
Effect of SNAP
Splenic arterioles. The addition of the NO donor SNAP abolished the myogenic response observed in the presence of L-NAME alone (Fig. 1C).
Wall-to-Lumen Ratio
The wall-to-lumen ratio (h/R) was greater in mesenteric (0.31 ± 0.01) than splenic (0.25 ± 0.003) arterioles. By contrast, h/R in the venules was greater in the splenic (0.35 ± 0.01) than in mesenteric vessels (0.24 ± 0.009). Wall thickness of the mesenteric venules (39.6 ± 0.8 µm) at 6 mmHg was significantly less than for the splenic venules (47.6 ± 1.1 µm).| |
DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Mesenteric arterioles exhibited myogenic responses, there being
increasing constriction as intramural pressure was raised above 60 mmHg
(Fig. 1A). By contrast, splenic hilar arterioles did not
demonstrate myogenic responses, except when NOS was inhibited (Fig.
1B). Neither mesenteric nor splenic veins exhibited myogenic responses (Fig. 3). However, the mesenteric venules were more distensible than splenic venules and more compliant in the
Ca2+-free medium. Although the splenic and mesenteric
vessels were of the same order (4th), the mesenteric vessels were
slightly smaller. One could argue that the failure of the splenic
vessels to show a myogenic response was attributable to this size
difference, there being some evidence in the literature that there is
an inverse relationship between the magnitude of the myogenic response
and vessel diameter (29). However, our data show clearly
that regardless of the vessel size (passive diameter at 60 mmHg),
myogenic responses were observed in the mesenteric arterioles and in
the splenic arterioles pretreated with L-NAME, but never in
the untreated splenic vessels (Fig. 4).
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The pressurized myograph and specific media used (Dulbecco's) were adapted from previously described protocols (11, 19, 29). Myogenic responses in small mesenteric arterioles have previously been reported by Sun et al. (29); the myogenic constriction of arterioles (<200 µm) we observed was almost identical to the responses they described in similar-sized arterioles. Thus an increase in mesenteric perfusion pressure would elicit myogenic constriction of the small arterioles to buffer and maintain mesenteric microvascular pressure relatively constant. Any increase that was relayed to the postcapillary circulation would be accommodated in the highly distensible mesenteric venous beds. By contrast, we propose that the absence of myogenic constriction in the splenic arterioles would allow an increase in perfusion pressure to be transmitted to the microvasculature, thus raising the driving force for fluid extravasation. The increase in microvascular pressure would furthermore be maintained by the failure of the splenic outflow vessels, the venules, to distend. Although we cannot exclude the possibility that the myogenic response in the spleen was shifted to smaller diameter vessels within the parenchyma of the organ, our data are not suggestive of such a proposition (Fig. 4).
Our studies are in agreement with those of Scotland et al. (25) that, although mesenteric arterioles normally exhibit a pronounced decrease in vessel diameter in response to an increase in intraluminal pressure, L-NAME enhances the myogenic response still further (6, 25, 31). By contrast, under normal conditions, the splenic arterioles exhibited no myogenic response. It was only on inhibition of NOS that the myogenic response was unmasked. This could not be attributed to an inherently weaker myogenic responses in the splenic arterioles because, in the presence of L-NAME, the magnitude of the pressure-induced reduction in vessel diameter was similar in both types of vessel (Fig. 1D). Rather, we propose that the myogenic response of splenic arterioles is normally completely masked by the vasodilatory response to basal NO release. Our previous studies report that splenic arterioles demonstrate greater sensitivity than do splenic venules to NO (1). These current results confirm that splenic arterioles are extraordinarily responsive to the vasodilatory activity of NO.
The mesenteric venules behaved as would be expected of capacitance vessels: diameter increased markedly with increasing intraluminal pressure. In the presence of Ca2+, the mesenteric venules also exhibited some vascular tone, so that distension was limited at higher intraluminal pressures. Previous studies of mesenteric veins have only investigated passive responses in Ca2+-free media, i.e., compliance (11). Those data differed slightly from our results; they reported higher mesenteric vascular compliance than we found, and their vessels continued to increase in diameter linearly, even at very high intraluminal pressures. Interestingly, we have noted that any damage to vessels (indicated by leak at the end of the experiment) was similarly characterized by unlimited compliance. Studies by Dornyei et al. (8) in skeletal muscle showed a similar pattern of response to our mesenteric venules, at similar pressure ranges. In our study we ensured that venules were handled delicately, not overstretched, and did not exhibit any signs of damage at the end of the experiment. We also used Dulbecco's medium as opposed to physiological salt solution (PSS). Myogenic responses and vascular tone can be maintained for long periods of time in Dulbecco's medium [>6 h, (19)]. Without careful treatment of veins and appropriate perfusion fluids, measurement of compliance and myogenic responses may not be reliable. Our data were also in agreement with a number of previous studies suggesting that venules are capable of generating vascular tone (2, 5, 8).
Myogenic responses had not been previously studied in splenic hilar vessels. As predicted, there was no myogenic response in the arterioles. However, contrary to our hypothesis, neither did the splenic venules exhibit myogenic constriction, although they did show evidence of vascular tone. However, the most striking factor probably contributing to the ability of the spleen to maintain an increase in microvascular pressure was the very low compliance of the splenic venules. At 4 mmHg, which is the lower end of the physiological range in splenic venules (27), splenic and mesenteric venular diameters were similar. As intraluminal pressure was increased, splenic venules failed to increase their diameter, this being quite unlike the behavior of the mesenteric venules. Such characteristics would serve to limit the decrease in outflow resistance as perfusion pressure is increased.
The splenic arterioles were characterized by a lower wall-to-lumen ratio than the mesenteric arterioles. This probably contributes to, but does not entirely account for, the reduced myogenic responses we observed in the splenic vessels. By contrast, in the venules, we identified a higher wall-to-lumen ratio in the spleen than in the mesentery. This is consistent with a previous report that these vessels are well endowed with vascular smooth muscle (22). Moreover, we have previously shown that splenic venules constrict both to ANF and to phenylephrine (1, 27). This suggests that, in addition to their low compliance, splenic venules also have a significant potential for constriction, and the ability to actively resist increases in diameter after an increase in intraluminal pressure (26).
In conclusion, splenic arterioles exhibit attenuated myogenic responses compared with mesenteric arterioles of the same order, possibly due to increased release of and/or reactivity to NO, and reduced smooth muscle cells in the vessel wall. Splenic hilar venules are also markedly less compliant than mesenteric venules. We propose that the decreased myogenic responses in the splenic arterioles coupled with low compliance in the venules allows increases in splenic perfusion pressure to be transmitted to the microvasculature and promotes increased fluid extravasation.
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ACKNOWLEDGEMENTS |
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This research was supported by a grant from the Canadian Institutes for Health Research. Z. L. S. Brookes is a Canadian Hypertension/Canadian Institutes of Health Research Fellow.
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FOOTNOTES |
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Address for reprint requests and other correspondence: S. Jacobs-Kaufman, 475 Heritage Medical Research Centre, Univ. of Alberta, Edmonton, Alberta, Canada T6G 2S2 (E-mail: susan.jacobs{at}ualberta.ca).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
First published February 27, 2003;10.1152/ajpregu.00411.2002
Received 10 July 2002; accepted in final form 7 January 2003.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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, passive response in Ca2+-free
medium; 
, active response in presence of
L-NAME plus SNAP. Vertical bars delineate SE.
* P < 0.05, significant decrease
compared with maximum diameter (myogenic response).
# P < 0.05, significant effect of
L-NAME on active response (
