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In spontaneously hypertensive rats, the pressure-distensibility curve of muscular arteries is shifted to higher pressure levels due to enhanced smooth muscle contractility, whereas venous elasticity remains unchanged.
Incremental compliance and distensibility of certain muscular arteries were recently reported to be normal or slightly increased in hypertension at the same pressure levels. In this work biomechanical properties of isolated perfused and superfused veins and large muscular arteries from saphenous bed from male spontaneously hypertensive (SHR) and Wistar–Kyoto (WKY) rats were compared in vitro. Outer diameter of cylindrical vessel segments was measured and intraluminal pressure (IP) was changed cyclically. We found larger contractile response to methoxamine (1.06×10−5 mol/l) in SHR arteries compared to WKY (active strain e.g. at 100 mmHg IP: 7.12±4.1 vs 0.35±0.46%). Resting incremental distensibility was higher (e.g. 100 mmHg IP: 3.4±0.4×10−6 vs 1.2±0.3×10−7 m2/N), elastic modulus lower (e.g. 100 mmHg IP: 3.7±0.6×105 vs 27±7.6×105 N/m2) in the arteries from SHR in pressure range of 60–110 mmHg. After papaverine administration (2.8×10−4 mol/l) the artery became more rigid, thus the increased incremental elasticity of SHR artery might be due to the enhanced smooth muscle tone. However, compared at in vivo pressure levels the differences were negligible suggesting a shift in the elastic parameters toward the higher operation pressures. Saphenous vein of SHR had larger diameter, than that of WKY, while in the wall thicknesses no difference were found (therefore external radius-wall thickness ratio was larger, e.g. at 6 mmHg IP: 15.9±3.0 vs 8.1±0.7). Consequently, lumen capacity of the vein was also higher in SHR, however, elastic parameters did not exhibit significant differences. We conclude that pressure-distensibility curve of muscular type arteries like SHR saphenous artery is shifted to higher pressure levels compared with that of normotensive controls. This shift is due to the enhanced smooth muscle contractility. The unchanged elasticity of veins suggests that the arterial deformations in SHR are not primary but secondary alterations.
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Szentiványi et al. (1998) studied this question.
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