Abundant evidence indicates that caveolae, caveolin-enriched lipid raft domains in the plasma membrane, are sites that concentrate entities involved in regulation of cardiovascular cells, including myocytes, fibroblasts and endothelial cells. Endothelial nitric oxide synthase (eNOS, NOS3) is the best-studied such entity but substantial data exist for many other types of molecules, including transporters, receptors and post-receptor components involved in signal transduction. However, many questions are unanswered regarding the basis for localization and maintenance of entities within caveolar microdomains. In addition, the contribution to caveolae to pathophysiology, other than of mutated caveolins in certain muscular dystrophies, is ill-defined. Our recent evidence indicates that SUMOylation (linkage of Small Ubiquitin-like Modifier) is a previously unappreciated modification of caveolin that occurs in cardiac myocytes and influences expression of β2-adrenoceptors, but not that of β1-adrenoceptors or eNOS. SUMOylation of β2-adrenoceptors alters receptor stability and turnover by catecholamines, including by catecholamines present in serum used for the growth of cells in vitro. Our results thus identify SUMOylation as contributing to the regulation of expression of certain partners and suggest that a “SUMOylation code” may help determine localization and stability of binding partners with caveolins in cardiovascular cells.