Growth responses in the arterial wall.

Arterial structural changes play a key role in atherosclerosis and hypertension and could become a valid target for pharmacotherapy of these disorders. Current insights in arterial growth control were derived from experiments in cell culture and in experimental animals. In this study, we evaluated growth responses in isolated arterial segments and compared our in vitro observations to arterial changes in experimental models of essential and secondary renal hypertension. In isolated renal artery segments, serum growth factors caused a transient stimulation of DNA synthesis in the arterial media. This in vitro growth response did not lead to media hyperplasia, hypertrophy or hyperploidy. In intact, conscious 6-week-old spontaneously hypertensive rats (SHR), DNA synthesis in the media of large arteries was two to four times larger than that in arteries of age-matched normotensive rats. Yet, the elevated wall/lumen ratio in renal arteries of adult SHR was due to a reduction of the arterial lumen diameter and not to an altered media cross-sectional area. In addition, while aorta-coarctation resulted in a marked increase of renal arterial cross-sectional area it did not alter the number of renal artery smooth muscle cells. These observations indicate that even powerful chemical and mechanical mitogenic conditions do not alter the number of medial smooth muscle cells. This could be due to rapid down-regulation of arterial growth responsiveness, migration, and turnover of cells.