T lymphocytes inhibit the vascular response to injury.

The proliferation of vascular smooth muscle cells is controlled by specific growth factors and cytokines acting in paracrine networks. Macrophage products such as the platelet-derived growth factor and interleukin 1 promote smooth muscle proliferation and are released in the arterial wall during atherosclerosis and repair processes. T lymphocytes are also present in vascular tissue, but their role in vascular growth control in vivo has been unclear.

Proliferation of smooth muscle cells in the inner and outer layers of the tunica media of arteries: an in vitro study.

During the development of atherosclerotic and fibromuscular proliferates/lesions, smooth muscle cells (SMC) in the media, particularly near the lumen, are activated to migrate into the intima, where they continue to proliferate to form an intimal thickening. It is to date unclear whether SMCs situated adjacent to the adventitia possess a lower capacity to proliferate because they are a special subpopulation of medial SMCs or because the adventitia excerts an inhibitory effect. We have, therefore, developed an in vitro system whereby we have attempted to clear up this uncertainty.

Fibromuscular proliferates induced in vitro using a trans-filter culture system.

A trans-filter co-culture system of vascular smooth muscle cells (SMC) and endothelial cells (EC) is compared with a trans-filter culture of SMC without EC. Explants from the tunica media of rabbit aorta are cultured on one side of a polycarbonate filter with a defined pore size (5 microns). Smooth muscle cells grow out from the media explants and migrate through the filter pores to the other side of the filter, where they proliferate.

Calcium antagonists and atherosclerosis.

Numerous trials have used calcium antagonistic substances to inhibit or prevent genesis and progression of atherosclerosis, as well as disintegration of intimal proliferates and calcium deposition in atheromas or in matrix tissue of artery walls. In experimental models, various components involved in the development of atherosclerosis can be influenced by calcium antagonists. Transendothelial transport through interendothelial spaces and through the endothelial cells are sensitive to calcium antagonists of various types.

Alpha 1-receptor antagonists urapidil and prazosin inhibit neointima formation in rat carotid artery induced by balloon catheter injury.

Sympathetic nerves and catecholamines seem to have a trophic influence on vascular smooth muscle cells in vivo. We therefore tested whether alpha 1-antagonists would inhibit proliferation in arterial smooth muscle in vivo. Smooth muscle cells were stimulated to form a neointima in rat carotid arteries after deendothelialization by means of a 2F embolectomy catheter.