The central nervous system and atherogenesis: role of the arterial smooth muscle cell

Within the last 2-3 decades neuropsychological factors have assumed a role of importance in atherogenesis implicating a contribution from the CNS to the development of arterial lesions. Despite extensive documentation in clinical studies, little work has been performed with experimental animals which could elucidate underlying mechanisms. Employing hypothalamic stimulation (HS) to model the role of the CNS, experiments in the author's laboratory have shown that atherosclerotic lesions develop in time. Evidence is presented that the underlying mechanism is due to vasospasm associated with proliferation of intimal arterial smooth muscle cells (ASMC). Both, the vasospastic and proliferative responses may originate with the same hypothalamic signal. The vasospastic response compromises perfusion, but by injuring the vessel produces pathology which increases the resistance of the artery to further spasm. The proliferation of ASMC which provides the elements for this 'stiffening' process also helps restore the vascular tone necessary to maintain the important function of perfusion. Atherosclerosis, therefore, may represent an adaptive response to excessive spasm which in many instances has advanced too far.