“…Wallingford and associates described that Prcp-null mice had elevated levels of alpha-MSH1-13 in the hypothalamus and were leaner and shorter than the wild-type controls on a regular chow diet. Prcp null mice were also resistant to high-fat diet-induced obesity Soisson and associates described the crystal structure of human PRCP E112D polymorphism in the prolylcarboxypeptidase gene was found to be associated with blood pressure response to benazepril in Chinese hypertensive patients Javerzat and associates described overexpression of PRCP during the intermediate phase of the chick chorio-allantoic membrane Recombinant PRCP (rPRCP) metabolized BK1-8 to BK1-7, whereas rPRCP was ineffective in metabolizing BK 1-9 PRCP was found to be active in human cerebrospinal fluid Overexpression of angiotensin type 2 (AT2) receptor in mouse coronary artery endothelial cells was found to increase expression of PRCP, which may contribute to kinin release PRCP is a 4OHTAM resistance factor in estrogen receptor-positive breast cancer cells PRCP gt/gt mice were found to be hypertensive and prothrombotic (Sorrells and Erdos, 1971) (Odya et al, 1978) (Skidgel et al, 1981) (Deddish et al, 1990) (Tan et al, 1993) (Tamaoki et al, 1994) (Suzawa et al, 1995) (Suga et al, 1995) (Jackman et al, 1995) (Watson, Jr. et al, 1997) To deal with proper delivery of blood to the tissues as well as many types of insults, including chemical and physical damage as well as infection, the cardiovascular system has evolved an intricate multilayer of specialized biochemical pathways. Multiple feedback mechanisms controlling blood flow with contrasting effects regulate normal vascular function, which have either stimulatory or inhibitory effects.…”