Canine Aortic Smooth Muscle Cells (CnAOSMC) are derived from tunica intima and tunica media of normal canine aorta. They are cryopreserved at second passage and can be cultured and propagated at least 10 population doublings. Platelet-derived growth factor (PDGF) is a potent mitogen and chemotactic agent which may be involved in intimal hyperplasia and atherosclerosis. It was shown that significant regional difference in PDGF production in normal canine aorta, and that SMC are a significant contributor to the regional variation in PDGF production¹. It was also shown that nebivolol relaxes vascular smooth muscle by NO- and cyclic GMP-dependent mechanisms². Graft SMCs are functionally altered producing more platelet-derived growth factor (PDGF) than aortic SMCs. PDGF produced by graft SMCs may contribute to the development of intimal hyperplasia³. Graft SMCs have decreased proliferation response, but have similar migratory response to PDGF compared with aortic SMCs⁴. Intrinsic differences in endothelial cells from proximal aorta versus the distal aorta have different capacity to produce PDGF in response to stimulants whereas unstimulated SMCs did not exhibit regional variation in PDGF production and did not increase PDGF secretion after PMA or thrombin teatment⁵. Identification of the cDNA for canine isoform of nitric oxide synthase (iNOS) can be used in the study of allograft rejection and cardiovascular disease⁶.