Vascular smooth muscles communicate and modulate blood flow and resistance throughout the body. Areteries have more smooth muscle, that's why they're thicker. They need to pump, veins need to receive and return. Both arteries and veins have the same endothelial lining (directly over the smooth muscle cells) which communicate and signal the vascular smooth muscles to contract or expand...
Vascular smooth muscle contracts or relaxes to both change the volume of blood vessels and the local blood pressure, a mechanism that is responsible for the redistribution of the blood within the body to areas where it is needed (i.e. areas with temporarily enhanced oxygen consumption). Thus the main function of vascular smooth muscle tonus is to regulate the caliber of the blood vessels in the body. Excessive vasoconstriction leads to hypertension, while excessive vasodilation as in shock leads to hypotension.
Here's a great paper which looked at the differences between venous and arterial smooth muscle cells (SMC)-
The differentiation state of SMC has been implicated in various vascular pathologies such as atherosclerosis [9,17] and intimal hyperplasia [10,11]. The dedifferentiated phenotype for venous SMC reported in this study is consistent with the cellular behavior characterized by increased proliferation, migration, and synthetic capabilities. Our results show increased levels of collagen synthesis and gelatinase activity in venous SMC. Collagen synthesis and accumulation are integral aspects of vascular repair [14,18]. Previous studies have also shown that gelatinase activity is a critical component of SMC migration in vein graft disease  and the formation of intimal hyperplasia after arterial injury and in vein grafts [14,20,21].
We see this remodeling in vein graft surgeries, which tend to fail after time because of the SMC reaction. This is why surgeons aren't keen on replacing veins just yet....these grafts have a higher failure rate due to intimal hyperplasia from SMCs.
http://cardiovascres.oxfordjournals.org ... 3/702.full
Although the saphenous vein remains a commonly utilized conduit in coronary artery bypass grafting, it is often plagued by vein graft diseases such as fibrointimal hyperplasia and accelerated atherosclerosis within 5–10 years after surgery . The causes for vein graft diseases are multifold. Studies have shown that many factors such as surgical trauma  and hemodynamic changes [36,37] are important in the development of vein graft intimal hyperplasia. Furthermore, consistent with our in vitro results, venous SMC dedifferentiation and proliferation have been shown in vein graft intimal hyperplasia [10,11]. Based on our study, venous SMC have particular intrinsic characteristics that may contribute to the development of vein graft disease.
hope this help explain....it's definitely part of CCSVI, as Dr. Gabbiani's studies into the collagen remodeling of the smooth muscle cells of CCSVI veins has shown us. CCSVI jugular veins have stiffer, less plient linings.