Local production of prostaglandins in relation to mammary function at the onset of lactation in the goat.

1. Arterial and mammary venous concentrations of prostaglandins F alpha (PGF alpha), E (PGE) and the PGF alpha metabolite, 13,14‐dihydro‐15‐oxoPGF alpha (DHK‐PGF alpha) were studied during late pregnancy and the onset of lactation in conscious goats. Mammary secretion concentrations of PGF alpha and DHK‐PGF alpha were determined, and mammary blood flow, arterial plasma progesterone concentrations and milk composition were also studied. 2. A significant output of PGF alpha from the mammary gland into mammary venous blood was observed during late pregnancy; this output ceased near term. 3. Mammary output of DHK‐PGF alpha into venous blood began about 6 days prepartum, suggesting an increasing capacity of the gland to metabolize PGF alpha. 4. The concentration of PGF alpha in mammary secretion increased from about 4 days pre‐partum, that of DKH‐PGF alpha from about 12 days pre‐partum. 5. It is concluded that although total mammary output of PGF alpha decreases during late pregnancy and early lactation, the rate of mammary synthesis of PGF alpha increases and the PGF alpha is increasingly secreted into milk and metabolized to DHK‐PGF alpha within the mammary gland. 6. Unilateral treatment of one mammary gland in goats with the PGF 2 alpha analogue, Cloprostenol, at two dose levels from 2‐3 days pre‐partum to 1‐2 days post‐partum prevented the changes in milk [Na] that occur at term in untreated glands. At the higher dose, the normal rise in milk [citrate] was abolished and milk yield was reduced; these effects persisted after cessation of treatment. 7. It is suggested that PGF alpha may play a local inhibitory role in mammary gland function during late pregnancy. It is further suggested that PGF alpha could be the factor, or one of the factors, proposed by Linzell & Peaker (1974) to be responsible for local control of mammary epithelial permeability and possibly also for secretory rate.