Showing papers by "Stéphane Laurent published in 1998"

Fibronectin Expression and Aortic Wall Elastic Modulus in Spontaneously Hypertensive Rats

Abstract: Recent studies have shown that large-artery wall remodeling per se does not reduce distensibility in hypertension, indicating qualitative or quantitative changes in arterial components. The aim of the study was to determine in 1-year-old spontaneously hypertensive rats (SHRs) the changes in the elastic properties of large arteries, as assessed by the incremental elastic modulus (E(inc)), and the changes in the extracellular matrix, including fibronectin (FN) and alpha5beta1-integrin. The relationship between E(inc) and circumferential wall stress was calculated from in vivo pulsatile changes in blood pressure and arterial diameter by using a high-resolution echo-tracking system at the site of the abdominal aorta and in vitro medial cross-sectional area. E(inc)-stress curves and FN and integrin alpha5-subunit contents were determined for each animal. Mean stress and E(inc) were higher in SHRs than in Wistar rats. However, in a common range of stress, E(inc)-stress curves for SHRs were superimposable on those for Wistar rats, indicating that wall materials in both strains have equivalent mechanical behavior. Immunohistochemistry indicated that total FN, EIIIA FN isoform, and alpha5-integrin increased in the SHRs aortas without changes in elastin and collagen densities. Total FN was also increased in SHRs as determined by Western blot analysis. No differences in FN and alpha5-subunit mRNAs were detected between SHRs and Wistar rats. These results indicate that the aortic wall material of SHRs and Wistar rats have equivalent mechanical properties, although in SHRs it is subjected to a higher level of stress. By increasing cell-matrix attachment sites, FN may participate in the mechanical adaptation of both cellular and matrix components in SHRs.

Connection of Smooth Muscle Cells to Elastic Lamellae in Aorta of Spontaneously Hypertensive Rats

Abstract: We have recently demonstrated that in large arteries of spontaneously hypertensive rats (SHR), there is no increase of stiffness despite the increase in wall thickness, a sign of mechanical adaptation of the arterial wall to the higher level of stress. Because the dense plaques of smooth muscle are a major site of anchorage between the muscle cells and extracellular matrix, we determined by electron microscopy the distribution of dense plaques and their connections to elastic lamellae in the abdominal aorta of 1-year-old SHR and control Wistar rats. In vivo echo-tracking measurement of aortic distensibility and elastic modulus indicates a reduction of arterial stiffness in SHR compared with Wistar rats when they are studied over a common range of blood pressure. The media thickness to body weight ratio was higher in SHR than in Wistar rats. In the media, the percentage of sectional area occupied by extracellular matrix was not different between Wistar rats and SHR. The average number of dense plaques per muscle cell was not different between Wistar rats and SHR. However, the percentage of cell surface occupied by dense plaques was increased in SHR, and the percentage of cell surface connected to the elastic lamellae was twice as high in SHR compared with Wistar rats (9.4+/-1.5% versus 3.8+/-1.1%). These results suggest that the elastin network plays a major role in the mechanical adaptation of the arterial wall in SHR, not through variations of its total amount but through variations of the extent of anchorage to the muscle cells.

Smooth Muscle Tone and Arterial Wall Viscosity An In Vivo/In Vitro Study

Abstract: The relationships between steady and pulsatile pressures, smooth muscle tone, and arterial viscoelastic behavior remain a matter of controversy. We previously showed that arterial wall viscosity (AWV) was 3-fold lower in vivo than in vitro and suggested that in vivo active mechanisms could minimize intrinsic AWV to improve the efficiency of heart-vessel coupling energy balance. The aim of the present study was to determine the role of smooth muscle tone on AWV, under various levels of steady and pulsatile pressures, both in vivo and in vitro. AWV of rat abdominal aorta was studied first in vivo after bolus injections of phenylephrine (PE) or sodium nitroprusside (SNP), then in vitro in response to PE or SNP. In vitro, arterial segments were submitted first to steady pressure (0 to 200 mm Hg) by increments of 20 mm Hg, then to increasing levels of pulse pressure (20 to 50 mm Hg) at various mean arterial pressures (75 to 150 mm Hg). AWV was quantified as the area of the pressure/diameter relationship hysteresis, issued from the simultaneous measurements of pressure (Millar micromanometer) and diameter (NIUS echotracking device). In vivo, AWV increased after PE and decreased after SNP, in parallel with pressure changes. In vitro, AWV was not significantly influenced by PE and SNP. After both PE and SNP, AWV increased with pulse pressure but was not influenced by mean arterial pressure. At any given pulse pressure, AWV was higher in vitro than in vivo. The relation between AWV and pulse pressure was significantly steeper in vitro than in vivo. These results show that AWV is strongly influenced by steady and pulsatile mechanical load but not by smooth muscle tone, both in vivo and in vitro. Factors other than sustained smooth muscle activation should be explored to explain the minimization of AWV in vivo compared with intrinsic in vitro values.

Opposite Effects of Remodeling and Hypertrophy on Arterial Compliance in Hypertension

Abstract: Sustained hypertension is associated with a reduction in large artery compliance. However, we previously showed that, at the site of the radial artery, a distal muscular artery, the compliance of hypertensive patients was not significantly different from those of normotensive controls when the two groups were studied at their respective mean arterial pressures, despite increased wall thickness in hypertensives. To determine whether this paradoxical finding could be related to a specific pattern of geometrical changes, we studied arterial compliance in never-treated hypertensive patients characterized either by radial artery hypertrophy or remodeling, and compared them to normotensive controls. By analogy with Devereux’s classification for left ventricular hypertrophy, we defined remodeling as an increased thickness to radius ratio (h/r) and a normal vascular mass (VM), and arterial hypertrophy as an increased VM irrespective of the values of h/r. Internal diameter and wall thickness were measured at the site of the radial artery using a high resolution echo-tracking system. The lumen cross-section-pressure curve was determined from the two simultaneous and continuous recordings of arterial diameter and blood pressure. Then, the cross-sectional compliance (CC) pressure curve was calculated. Isobaric compliance was calculated at 100 mm Hg. Thresholds for h/r and VM were determined according to gender as the 95th percentile of a group of 100 normotensive subjects. The group of hypertensive patients included 58 patients with hypertrophy (h/r: 0.25±0.04;VM: 31±6 mg/cm; mean±SD) and 25 patients with remodeling (h/r: 0.29±0.06;VM: 20±4 mg/cm) and was compared to a group of 50 age- and gender-matched normotensives (h/r: 0.16±0.02;VM: 17±4 mg/cm). Compared to normotensives, isobaric compliance of the radial artery was increased in hypertensive patients with hypertrophy (HH) whereas it was not different in hypertensive patients with remodeling (RH). These results indicate that compliance is dependent on hypertrophy or remodeling pattern and suggest that in the face of hypertension, only arterial hypertrophy is an adaptive process leading to normal operating compliance through an increased isobaric compliance.