“…Both NA and AII stimulate prostaglandin synthesis in several tissues including the kidney (Gilmore et al, 1968;McGiff, et al, 1970;1972;Needleman et al, 1973;Mullane & Moncada, 1980;Shebuski & Aiken, 1980). The ability of prostaglandins, particularly PGE2 and PGI2, to reduce vascular reactivity to vasoconstrictor stimuli (Lonigro et al, 1973;Malik et al, 1980;Susic et al, 1981) and the demonstration that glucocorticoids inhibit prostaglandin synthesis in several intact cell systems and perfused organs (Kantrowitz et al, 1975;Tashjian et al, 1975;Lewis & Piper, 1975;Hong & Levine, 1976;Gryglewski, 1976;Herbaczynska-Cedro & Staszewska-Barczak, 1977;Blackwell et al, 1978;Zusman & Keiser, 1980) presumably by stimulating the synthesis of a phospholipase A2 inhibitor(s) (macrocortin, lipomodulin or renocortin) (Flower & Blackwell, 1979;Hirata et al, 1980;Cloix et al, 1983), has led to the proposal that glucocorticoids enhance vascular reactivity to NA by inhibiting the synthesis of PGE2 and PGI2 (Rascher et al, 1980;Axelrod, 1983).…”