Effects of Angiotensin II on the Growth of Vascular Smooth Muscle Cells.
10.4070/kcj.1999.29.2.209
- Author:
Kyung Man KIM
;
In Seop KIM
;
Su Je PARK
;
Wang Soo LEE
;
Hak Jin KIM
;
Sang Wook KIM
;
Tae Ho KIM
;
Chee Jeong KIM
;
Mi Kyung KIM
;
Wang Seong RYU
;
Un Ho RYOO
- Publication Type:Original Article
- Keywords:
Angiotensin ii;
Vascular smooth muscle cell;
Hypertrophy
- MeSH:
Angiotensin II*;
Angiotensins*;
Animals;
Blood Pressure;
Collagenases;
Hypertrophy;
Muscle, Smooth, Vascular*;
Myocytes, Smooth Muscle;
Pancreatic Elastase;
Radioactivity;
Rats;
Renin-Angiotensin System;
Saralasin;
Spectrum Analysis
- From:Korean Circulation Journal
1999;29(2):209-215
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: The octapeptide hormone of the renin-angiotensin system, angiotensin ii, regulates a wide variety of physiological responses including salt and water balance, blood pressure, and vascular tone. Contradictory results have been reported regarding the effects of angiotensin ii on vascular smooth mu-scle cell (VSMC) proliferation. The aim of the present study was to investigate the direct effect of angiotensin ii on the growth of VSMC. MATERIALS AND METHOD: Rat aortic smooth muscle cells were obtained by the combined collagenase and elastase methods. Cells between the 4th and 8th passages were used for the experiments. Cultures were treated daily for 3 days with either angiotensin ii alone or angiotensin ii with equimolar concentrations of saralasin. Incorporated radioactivity of [3H]thymidine and [14C]phenylalanine was measured by liquid scintillation spectrometry. RESULTS: Angiotensin ii increased [14C]phenyalanine incor-poration about 20-30%, and saralasin completely blocked the stimulation by angiotensin ii. However, there was no significant increase in [3H]thymidine incorporation by angiotensin ii stimulation in this study. CONCLUSION: These results suggest that angiotensin ii alone induces cellular hypertrophy but has no detectable mitogenic activity in cultured rat aortic VSMC.