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Circulation Research. 1995;77:823-831

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(Circulation Research. 1995;77:823-831.)
© 1995 American Heart Association, Inc.


Articles

Effect of Mechanical Forces on Growth and Matrix Protein Synthesis in the In Vitro Pulmonary Artery

Analysis of the Role of Individual Cell Types

Valeri Kolpakov, Mark D. Rekhter, David Gordon, Wei Hua Wang, Thomas J. Kulik

From the Department of Pediatrics (V.K., W.H.W., T.J.K.), Division of Pediatric Cardiology, and the Department of Pathology (M.D.R., D.G.), University of Michigan Medical School, Ann Arbor.

Correspondence to Dr Thomas J. Kulik, Division of Pediatric Cardiology, University of Michigan Hospitals, MCHC F 1310, Box 0204, Ann Arbor, MI 48109-0204.

Abstract The effect of mechanical stimuli on pulmonary artery growth and matrix tissue synthesis (and how individual cell types in the vessel wall respond to such stimuli) is incompletely characterized. Rabbit pulmonary arteries were placed in tissue culture medium and subjected to varying magnitudes of stretch or hydrostatic pressure (separately) for 4 days. The rate of protein synthesis in smooth muscle cells (by quantitative autoradiography) was positively related to the magnitude of stretch, as were the percentage of procollagen type I–positive cells and the rate of cell replication. In adventitial fibroblasts, stretch increased the rate of replication but not of protein synthesis. Hydrostatic pressure had little or no effect on the variables measured in either smooth muscle cells or fibroblasts. Stretch also increased the rate of elastin and collagen synthesis in the whole pulmonary artery segment, and after 4 days of stretch, the contents of actin and elastin were increased. Removal of the endothelium did not affect stretch-induced protein, collagen, or elastin synthesis but augmented stretch-induced smooth muscle replication. These data suggest that in the intact pulmonary artery, stretch, but not pressure, can stimulate hypertrophy and hyperplasia in smooth muscle cells and hyperplasia in fibroblasts. Matrix protein synthesis and accumulation are also increased by stretch. Neither stretch-mediated growth nor matrix protein synthesis required endothelium in this model.


Key Words: mechanical stress • growth • pulmonary hypertension • vascular smooth muscle • autoradiography




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