TY - JOUR
T1 - Effects of hypertension on morphological, contractile and mechanical properties of rat aortic smooth muscle cells
AU - Matsumoto, Takeo
AU - Yamamoto, Mitsunobu
AU - Seo, Shinji
AU - Sato, Junpei
AU - Kato, Yoko
AU - Sato, Masaaki
N1 - Funding Information:
This work was supported in part by Grant-in-Aid from the Ministry of Education, Science and Culture in Japan (Nos. 22240055 and 3218-22127008) and the Sumitomo Foundation.
PY - 2011/9
Y1 - 2011/9
N2 - We studied the effects of hypertension on morphological, contractile, and tensile properties of smooth muscle cells (SMCs) isolated from rat aortas. Male Wistar rats with induced Goldblatt hypertension had their thoracic aortas excised 16-24 weeks postoperatively to isolate SMCs by enzymatic digestion. Cell shape was measured before and after cell contraction induced by norepinephrine. Tensile properties of untreated SMCs were obtained with a laboratory- made micro tensile tester. The cell diameter was significantly larger (p<0.01) in hypertensive animals (9.2 lm) than age-matched controls (7.4 lm), while the length was not statistically different (55 lm). Cell contraction was significantly smaller (p<0.01) in hypertensive animals (7%) than controls (30%). The initial elastic modulus of SMCs was significantly smaller (p<0.05) in hypertensive animals (4.3 kPa) than controls (10.2 kPa). Wall thickening and reduction of contractility in hypertensive aortas was also observed in tubular segments of the aorta in rats exposed to hypertension for 16 weeks. The results showed that these changes also occurred at the cellular level, and they were accompanied by softening of the cells. Hypertension causes smooth muscle hypertrophy, which may decrease actin filaments as during the phenotypic transformation from acontractile to synthetic state, and thus may cause the inhibition of contractile properties and cell softening.
AB - We studied the effects of hypertension on morphological, contractile, and tensile properties of smooth muscle cells (SMCs) isolated from rat aortas. Male Wistar rats with induced Goldblatt hypertension had their thoracic aortas excised 16-24 weeks postoperatively to isolate SMCs by enzymatic digestion. Cell shape was measured before and after cell contraction induced by norepinephrine. Tensile properties of untreated SMCs were obtained with a laboratory- made micro tensile tester. The cell diameter was significantly larger (p<0.01) in hypertensive animals (9.2 lm) than age-matched controls (7.4 lm), while the length was not statistically different (55 lm). Cell contraction was significantly smaller (p<0.01) in hypertensive animals (7%) than controls (30%). The initial elastic modulus of SMCs was significantly smaller (p<0.05) in hypertensive animals (4.3 kPa) than controls (10.2 kPa). Wall thickening and reduction of contractility in hypertensive aortas was also observed in tubular segments of the aorta in rats exposed to hypertension for 16 weeks. The results showed that these changes also occurred at the cellular level, and they were accompanied by softening of the cells. Hypertension causes smooth muscle hypertrophy, which may decrease actin filaments as during the phenotypic transformation from acontractile to synthetic state, and thus may cause the inhibition of contractile properties and cell softening.
KW - Cytoskeleton
KW - Endoplasmic reticulum
KW - Golgi apparatus
KW - Hypertrophy
KW - Mechanical adaptation
KW - Phenotypic transformation
KW - Remodeling
UR - http://www.scopus.com/inward/record.url?scp=81855183218&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=81855183218&partnerID=8YFLogxK
U2 - 10.1007/s12195-011-0182-y
DO - 10.1007/s12195-011-0182-y
M3 - Article
AN - SCOPUS:81855183218
VL - 4
SP - 340
EP - 347
JO - Cellular and Molecular Bioengineering
JF - Cellular and Molecular Bioengineering
SN - 1865-5025
IS - 3
ER -