(Hypertension. 1997;29:1199-1203.)
© 1997 American Heart Association, Inc.
Articles |
Time Course Changes of the Mechanical Properties of the Carotid Artery in Renal Hypertensive Rats
From the Division of Hypertension, University Hospital, Lausanne, Switzerland.
Correspondence to Daniel Hayoz, Division of Hypertension, CHUV, CH-1011 Lausanne, Switzerland. E-mail daniel.hayoz{at}chuv.hospvd.ch
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Abstract |
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Abstract Distensibility of the carotid artery is not altered 2 weeks after renal artery clipping despite adaptive vascular hypertrophy related to hypertension. The purpose of this study was to assess arterial wall behavior with hypertension persisting for a longer period. Male Wistar rats were examined 1, 5, 9, and 24 weeks after renal artery clipping (two-kidney, one clip renal hypertension; n=40) or after sham operation (n=39). Mean blood pressure increased significantly to 132±4, 143±4, 153±4, and 144±4 versus 98±2, 107±2, 115±3, and 108±3 mm Hg, respectively, in 1-, 5-, 9-, and 24-week hypertensive rats and age-matched controls. Cardiac and vascular hypertrophy increased in parallel and were correlated to mean blood pressure. Wall stress at mean blood pressure did not differ between the hypertensive and normotensive groups (3.79±0.24, 4.60±0.34, 4.49±0.27, and 4.14±0.28 versus 3.15±0.12, 4.14±0.25, 4.80±0.28, and 4.69±0.32 103 dyne/cm2, respectively, in 1-, 5-, 9-, and 24-week hypertensive rats and age-matched controls). Distensibility-pressure data from the two groups fell on a common curve for all study periods. The intrinsic properties of the wall constituents were similar in controls and hypertensive rats at 1 and 5 weeks. However, the arteries became stiffer in the 9- and 24-week hypertensive rats, as illustrated by a shift to higher levels of the incremental elastic modulus–stress curve. Wall stress remains constant at mean blood pressure as a result of the increase in wall tissue mass. With time, even though the distensibility-pressure curve is not shifted downward, the thickened wall becomes stiffer in the hypertensive rats, which may predispose them to accelerated alterations of the wall material.
Key Words: hypertrophy • hypertension, renovascular • ultrasonography
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Introduction |
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Vascular hypertrophy of large vessels is one of the characteristic structural alterations occurring during chronic hypertension.1 2 3 Although hypertrophy attenuates the increase in wall stress caused by increased intravascular pressure, it may have a deleterious effect by increasing the stiffness of the artery. One of the main functions of conductance arteries is to smooth the pulsatile output from the heart and provide a continuous flow to the distal vascular beds. Indeed, if the arterial wall stiffens, this function is altered, resulting in an increased pulse pressure as a consequence of reduced arterial compliance and earlier wave reflection.4 However, in vivo determination of the mechanical properties of hypertrophied arteries has demonstrated that the isobaric distensibility of the carotid artery in spontaneously hypertensive rats5 6 7 8 9 and renal hypertensive rats9 10 is not decreased. Yet, whether this compensatory adaptation changes over a longer period of time has not yet been determined in the two-kidney, one clip (2K1C) model of renal hypertension. The aim of this study was to examine the time course effects of renovascular hypertension on the mechanical properties of the carotid artery at 1, 5, 9, and 24 weeks after clipping of the renal artery of Wistar rats. The distensibility-pressure curves of the common carotid artery were established in intact rats with an echotracking device combined with intra-arterial blood pressure (BP) monitoring.11 12 13 Morphometric examination was carried out for the determination of intima-media thickness and cross-sectional area of the common carotid artery followed by estimation of the incremental modulus of elasticity (Einc) and wall stress.
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Methods |
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Male Wistar rats weighing 170 to 210 g were obtained from Iffa-Credo. Animal care, surgical preparation, and experimental procedures were approved by the Government Review Committee for animal experiments. In half of the rats, a 0.2-mm-ID clip was placed on the left renal artery with rats under halothane anesthesia (Halothane BP, Arovet AG) (2K1C Goldblatt rats, n=40). A sham operation was performed in the other rats (sham rats, n=39). All rats were housed at a constant temperature of 23°C. Ordinary rat chow (UAR, A04) containing 100 µmol sodium/g and tap water were provided ad libitum.
Both clipped and sham-operated rats were divided into four
groups. The first group of 12 hypertensive and 8 control rats was
examined 1 week after the surgical procedure; the second group of 10
rats each, after 5 weeks; the third group of 8 hypertensive rats and 11
controls, after 9 weeks; and the fourth group of 10 hypertensive rats
and 10 controls, after 24 weeks. On the day of the experiment,
anesthesia was induced and maintained with halothane at a
concentration of 1.5%. The right common carotid artery was cannulated
with a catheter (PE-50, Portex) filled with a heparinized 0.9% NaCl
solution. Intra-arterial pressure and heart rate were
monitored with a computerized data-acquisition system as described
previously.14 The internal diameter of the left common
carotid artery was measured at the same time with an A-mode ultrasonic
echotracking device (Diarad, Asulab) that has already been used in
humans and animals.6 15 16 17 Briefly, the
apparatus consists of an A-mode ultrasonic echotracking
device that measures the variations in diameter of the common carotid
artery with a precision close to 1 µm. The high resolution
reached with this device is made possible by oversampling (5000
arterial diameter measurements per second) and averaging 16
consecutive values. A 10-MHz transducer is placed perpendicularly to
the arterial axis with Doppler mode, and an ultrasonic
gel is used for signal transduction. Arterial wall
movements that produce echoes of larger amplitude than those of
surrounding tissues are visualized on a screen and tagged by electronic
tracers. Ten successive diameter-pressure recordings were made
for each rat in a given 5-minute period and then averaged for
analysis. The simultaneous arterial
diameter and BP measurements were processed on-line to calculate a
diameter-pressure relationship, which is subsequently converted into an
arterial cross-sectional compliance-pressure curve
characterized over the whole range of operating BPs. This curve fits
best with an arctangent function described by Langewouters et
al.18 Cross-sectional compliance (C) in the case of a
cylindrical vessel is given by 
S/P, where S is the change in
cross section, and P is the change in BP. Arterial
cross-sectional distensibility (D) is the inverse of the Peterson
elastic modulus,19 ie, the compliance value normalized for
the cross section (S). It is defined as D=(1/S)x(S/P).
At the end of the measurements, the rats were euthanized with a lethal dose (90 mg/kg IV) of pentobarbital (CHUV). The heart was immediately excised, squeezed, and weighed.
The common carotid artery was pressurized and fixed at 100 mm Hg
during 30 minutes with intra-arterial infusion of a 4%
paraformaldehyde solution. The left common carotid
artery was then excised and cannulated with an adapted polyethylene
catheter to preserve a circular shape during processing for
histological examination. Paraffin-embedded tissue
blocks were sectioned at a thickness of 5 µm and stained by
hematoxylin-eosin. Histometric measurements were performed with a
microscope (Diaphot, Nikon). The intima-media thickness (IMT) and
internal diameter measurements were carried out with a 200-fold
magnification in a blinded fashion. The measurements from two carotid
sections and six fields per section were averaged. The intima-media
cross-sectional area (CSA) of the fixed arteries was determined
according to the formula CSA=
[(Internal
Radius+IMT)2-(Internal Radius)2]. The
media-to-lumen ratio was calculated according to the formula
Media-to-Lumen Ratio=IMT·100/Internal Radius.
For estimation of Einc and mean circumferential stress, arterial wall thickness was derived for each level of BP from the cross-sectional area measured at histology and from the internal diameter (d) measured in vivo. As the arteries are pressurized during fixation, longitudinal retraction is prevented. It is further assumed that the cross-sectional area remains constant in vivo and in vitro and thus is not influenced by changes in diameter because of the incompressibility of the wall material.11 20 However, because of dehydration of the fixed tissue, the calculated thickness underestimates in all groups the real value of the nonfixed artery (personal observations, unpublished data, 1996). Calculation with this value leads to an overestimation of Einc and mean circumferential stress. However, it could be assumed that the overestimation is present to the same degree in all arteries; thus, these parameters were compared among the groups.
Wall thickness (h) was calculated according to the formula
h=
{[CSA+(d/2)2]/}-d/2. Circumferential
stress (
) at each level of operational BP (p) and internal diameter
(d) was derived from the formula =pd/2·h. Finally,
Einc was defined as
Einc=
/Strain=(n+1)-n/[d(n+1)-dn]
and was calculated for each increase in intra-arterial BP
of 2.5 mm Hg within the operational BP range.
Statistical Analysis
Between-group comparisons of body weight, heart weight index
(heart weight [milligrams] divided by body weight [grams]),
diameter, distensibility, Einc and mean circumferential
stress of the carotid artery at mean BP, internal diameter at
histology, cross-sectional area, intima-media thickness, media-to-lumen
ratio, and BP were made by the Bonferroni/Donn test adapted for
multiple comparisons. The diameter-pressure and distensibility-pressure
curves were established within operating pressures, the upper and lower
limits representing the mean systolic and
diastolic values for the group, respectively. For
statistical evaluation of the Einc-stress curves, the areas
under the curves of the overlapping stress ranges were compared with
Scheffé's S test. Results are given as mean±SEM.
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Results |
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Body weight increased with time, and renal artery clipping did not alter growth in hypertensive compared with sham-operated rats except in the 24-week hypertensive rats (Table 1
). One
week after clipping, BP was significantly higher in the hypertensive
than the sham-operated rats. BP of the hypertensive rats remained
significantly higher up to 24 weeks. Over time, mean BP was similarly
increased by 33% to 35% in all hypertensive groups compared with
values in the respective controls. Pulse pressure was enhanced in the
hypertensive rats at 1, 9, and 24 weeks after clipping. Cardiac
hypertrophy was apparent as early as 1 week after clipping
and persisted at 5, 9, and 24 weeks after clipping.
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At histological examination, the intima-media thickness
and media-to-lumen ratio of the carotid artery were increased in all
hypertensive compared with sham-operated rats (Table 2).
Intima-media cross-sectional area was also significantly increased in
the hypertensive rats, and the percent rises compared with age-matched
controls were 39%, 51%, 65%, and 90% at 1, 5, 9, and 24 weeks
after clipping, respectively.
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Since the operating BPs did not overlap in hypertensive and
sham-operated rats, the mechanical properties of the carotid artery
could not be compared in the range of their respective operating BPs
(Figure). However, at least at 1, 9, and 24 weeks after
clipping, the distensibility-pressure curves of the hypertensive rats
did not appear to be shifted toward lower levels compared with curves
in the controls. Five weeks after clipping, the curve appeared to be
shifted to higher levels. When distensibility and internal diameter
were analyzed at mean operating BP, arterial
distensibility was significantly decreased (P<.05) and the
internal diameter increased (P<.05) in all hypertensive
rats compared with their respective controls (Table 3).
Wall stress at mean BP was not different between normotensive and
hypertensive rats. However, Einc was increased in the
hypertensive rats at all ages compared with controls at mean BP levels.
When Einc was plotted against wall stress, in the 1- and
5-week hypertensive rats, the curves did not differ from those of the
controls (Fig 1). However, 9 weeks after clipping, the curves were
significantly steeper, revealing stiffening of the intima-media
material. The difference between the Einc-stress curves was
even more pronounced in the 24-week rats.
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Discussion |
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The 2K1C Goldblatt rat model of renal hypertension rapidly develops a very severe form of hypertension.21 As early as 1 week after clipping of the renal artery, the rats exhibit high BP associated with vascular and cardiac hypertrophy. Over time, BP increases further, associated with increasing vascular hypertrophy. The carotid artery undergoes eccentric hypertrophy rather than typical remodeling known to occur with chronic hypertension in the resistive vascular territory. Indeed, the lumen of the vessels did not decrease throughout the experiment while the arterial wall thickened. An important consequence of this hypertrophic process is the normalization of wall stress, as shown in the present experiment. By analogy to myocardial adaptation to increased aortic impedance, the eccentric hypertrophy of the vascular wall may be regarded as an adaptive mechanism to normalize wall stress. However, thickening of the media may enhance metabolic alterations, such as increasing free radical production, that may predispose to atherosclerosis.22 23 Although the adaptive mechanisms prevent a shift to lower levels of distensibility-pressure curves in this hypertensive rat model for the four periods considered in the present study, they are not sufficient to maintain distensibility at control levels at the higher operating BP. These results are in disagreement with previous work showing a decreased compliance of the rat carotid artery after 8 weeks of renal hypertension.24 However, these results were obtained in a static in situ model and therefore cannot be compared with the present in vivo dynamic measurements.
One week after clipping of the renal artery, vascular hypertrophy of the carotid has already occurred, without reduction of its isobaric distensibility. On the contrary, the distensibility-pressure curve is shifted slightly upward compared with that of control rats. This clearly demonstrates that the arterial distensibility reflects the combined effect of geometric parameters such as diameter and wall thickness and intrinsic wall properties defined by Einc. Only the determination of the latter parameter is indicative of the alterations of the wall constituents. Since the intraluminal pressure is perceived by the wall material as a pressure-induced stress, Einc is best determined for a given circumferential wall stress.25 The Einc plotted against wall stress after 1 week is not different between the two groups of rats.
At 5 weeks, with a further increase in BP and vascular hypertrophy, the distensibility-pressure curve shows a more pronounced trend toward higher levels than at 1 week. Although isodistensibility is not achieved at 5 weeks for operating BPs in the hypertensive rats, our results demonstrate that besides an increase in wall tissue mass, additional adaptive transformations result in a decreased stiffness of the arterial wall expressed by the Einc at isobaric conditions (data not shown). At week 5, again the Einc plotted against wall stress shows similar values for a given level of stress for the two populations.
The adaptive process observed in the early phase of this study deserves two comments. First, the extremely rapid increase in cardiac and vascular mass may result from the synergistic effects of the activated renin-angiotensin system and its accompanying high BP and the growth conditions of these young rats. Up to 5 weeks, the adaptation shows an autoregulation, with thickening of the vessel wall and reduced stiffness of the material at isobaric conditions. These results confirm our previous observations in the 2K1C Goldblatt rat model and provide new information on the intrinsic properties of the vascular wall while adapting to an increased BP. These results are also very similar to those observed in the radial arteries in newly diagnosed hypertensive patients who exhibit vascular hypertrophy, preservation of isobaric arterial distensibility, and similar Einc values at equivalent stress levels compared with control subjects.26
In contrast to the early adaptive phase, 9 and 24 weeks after clipping, the arterial wall shows a different evolution. Indeed, Einc plotted against wall stress shows a significantly increased stiffness of the carotid in the hypertensive compared with the control rats even though the distensibility-pressure curve was not shifted to lower levels. Thickening of the vessel wall without changes in internal diameter, ie, eccentric hypertrophy,26 at weeks 9 and 24 explains the different Einc-stress curves between the two rat groups while the distensibility-pressure curves remain similar. Thus, it appears that with a longer duration of hypertension, the constituents involved in the thickening of the artery become significantly more rigid than those of the carotid artery of control rats for equivalent wall stress levels as a result of either quantitative or qualitative modification of the individual wall components. These results clearly emphasize the need to characterize arterial biomechanics with indexes discriminating those dependent in part on geometric changes (compliance and distensibility) from those relative to intrinsic elastic property changes (elastic modulus). If determination of arterial compliance allows one to estimate the buffering capacity of the artery, it does not provide any qualitative information on the wall material at risk of undergoing atherosclerotic transformations, as shown here between weeks 1 and 24. The second phase of adaptation seen here at 9 and 24 weeks is reminiscent of the aging process observed in human large conduit vessels. In contrast to the preserved or increased arterial distensibility accompanying vascular hypertrophy of newly diagnosed hypertensive patients, aging is characterized by hypertrophic vessels with decreased distensibility.27 Thus, at 9 and 24 weeks, a combination of the hypertension-induced alterations and aging or accelerated fatigue may be responsible for the increased rigidity of the wall material at equivalent wall stress but without a decline in the distensibility-pressure curve. The strong correlation between the degree of hypertrophy and BP indicates once again that the increase in BP per se may be a potent stimulus for the development of the hypertrophy. Since plasma renin activity was not measured, the contribution of an activated renin-angiotensin system on vascular hypertrophy could not be evaluated. However, on the basis of previous studies, plasma renin activity rises in the 2K1C rat for more than 12 weeks after clipping.28 29 Thus, it can be assumed that at 9 weeks, plasma angiotensin levels were still increased and may have contributed to the progression of vascular hypertrophy. However, in the long run, despite protective adaptations, accelerated alterations of the wall material caused by high BP and aging lead inevitably to stiffening of the arterial wall. Reversibility of the morphological changes in this second phase may become more hypothetical.
In conclusion, the 2K1C Goldblatt rat model of renal hypertension develops a very severe form of hypertension, with early cardiac and vascular hypertrophy. Parallel to the hypertrophic process, the intrinsic properties of the arterial wall remain normal up to 5 weeks after clipping but become clearly stiffer after 9 weeks for similar levels of wall stress. Nevertheless, these results demonstrate that the carotid arterial wall can adapt to increased intra-arterial pressure by normalizing wall stress and maintaining a relatively normal distensibility-pressure curve. Further studies analyzing the effect of the initiation of blood pressure–lowering therapy at different stages of wall adaptation may provide useful information on the reversibility of morphological and functional alterations.
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Acknowledgments |
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This work was supported by grants from the Swiss National Science Foundation (No. 32-42515-94). D.H. is supported by a career award from the Max Cloetta Foundation.
Received August 5, 1996; first decision September 3, 1996; accepted November 18, 1996.
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