Abstract-Our aim was to determine the structural factors that determine the mechanical adaptation of the carotid arterial wall in stroke-prone hypertensive rats (SHRSP). Distensibility-pressure and elastic modulus-stress curves assessed by in vivo echo-tracking measurements indicated a reduction in arterial stiffness in 13-week-old SHRSP compared with Wistar-Kyoto rats (WKY). Elastin and collagen contents determined biochemically were not different between SHRSP and WKY. Confocal microscopy showed that the mean area of fenestrations and fraction of area occupied by fenestrations of the internal elastic lamina (IEL) were smaller in SHRSP than in WKY, which indicated a reduction in stress-concentration effects within the IEL. Immunohistologic staining of EIIIA fibronectin isoform and total fibronectin (also as determined by Western blot) was greater in SHRSP, which suggested increased cell-matrix interactions. We suggest that these structural modifications of the vascular wall play a synergistic role in the mechanical adaptation to a high level of stress in SHRSP. (Hypertension. 2001;37:1101-1107.)Key Words: arteries Ⅲ elastin Ⅲ lamina, internal, elastic Ⅲ fenestrations Ⅲ fibronectin Ⅲ remodeling Ⅲ hypertension, experimental S pontaneously hypertensive rats of the stroke-prone substrain (SHRSP) are considered to be a good model for severe hypertension associated with increased cerebrovascular fragility. 1 In elastic arteries, recent study has demonstrated that distensibility of the carotid artery is increased in SHRSP compared with that in Wistar-Kyoto rats (WKY) for a given arterial pressure level (AP). 2 This finding suggests a mechanical adaptation of the arterial wall, which indicates qualitative or quantitative changes in arterial components.Elastin plays a major role in determining mechanical properties of the vascular wall. Elastic lamellae of large arteries were fenestrated, as well illustrated by electron microscopy. [3][4][5] More recently, confocal microscopy has shown that an enlargement of these fenestrations in the internal elastic lamina (IEL) during development contributes greatly to vascular wall remodeling induced by the increase in blood flow. 6 The influence of these fenestrations may be explained by stress-concentration phenomena: enlarged fenestrations concentrate stresses in the immediately adjacent tissue, which induces vessel development. 4,7 In chronic hypertension, mean circumferential wall stress is most often increased, despite the development of arterial wall hypertrophy. 8 -10 Consequently, an adaptive response that was able to limit stress-concentration effects in the IEL would be a reduction in size and total area of fenestrations in the IEL.We have suggested that stress-induced activation of the muscle cell, which causes enhanced synthesis of the adhesion protein fibronectin (FN) in SHR, is such a response. 11 By increasing cell-matrix attachment sites, the accumulation of FN may alter distribution of wall stress within the arterial wall and play an important role in regulation o...

The desmin is essential to maintain proper viscoelastic properties, structure and mechanical strength of the vascular wall.

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. (Hypertension. 1998;32:360-364.)Key Words: viscosity Ⅲ arteries Ⅲ muscle, smooth Ⅲ sodium nitroprusside Ⅲ phenylephrine Ⅲ aorta A lthough it is well known that biological tissues, including the arterial wall, respond to stress through both elastic and viscous behaviors, the viscous aspect has often been neglected. Indeed, authors acknowledged the theoretical difficulties raised by taking viscosity into account and the methodological difficulties for measuring it.1,2 In most studies, viscosity was considered a dampening phenomenon and expressed in term of phase delay. An alternative approach, developed by mechanical engineers, was to consider viscosity an energy-dissipating phenomenon during the mechanical transduction.3-5 Indeed, a major function of large arteries is to store mechanical energy generated by the heart during systole and to restore it during diastole to optimize the heart-vessel coupling. [6][7][8][9] We used this approach in a recent study 10 and showed that the viscosity measured in vivo in intact animals was 3-fold lower than viscosity measured in vitro at the same arterial site under similar pressure conditions. We hypothesized that active mechanisms...