Exposure of vascular smooth muscle cells to AVP also increases smooth muscle actin through activation of all three MAP kinase family pathways. Because AVP has the ability to regulate and increase smooth muscle actin this suggests that AVP may not only regulate growth of vascular smooth muscle but also promote expression of smooth muscle-specific contractile proteins . Previous studies have shown that AVP can produce an exaggerated vascular vasoconstriction in young spontaneously hypertensive rats (SHR) relative to normotensive rats. This exaggerated response was likely associated to a higher density of V1 receptors associated with increased AVP gene expression. Finally AVP and other neuropepetides have been shown to serve as autocrine growth factors for some solid tumors. The mitogenic influence of AVP is thought to involve increases in intracellular calcium. AVP is often expressed in small cell lung cancer (SCLC), and can act as an autocrine growth factor in these cancers. AVP expression in SCLC is thought to be dependent on the modulation of normal repressor activity 12. Because AVP has been implicated in the physiology of vascular constriction and mean vascular pressure, and also because it has been shown to be expressed in certain types of cancer, it may also have a role as an angiogenic factor in intratumoral vascularization in ovarian cancer carcinogenesis. It is the purpose of our proposed study to investigate the relationship between AVP expression and its vascular receptor with ovarian neoplasm histology.