and calcitriol and decreased insulin responsiveness or insulin resistance likely affect mineral homeostasis and bone metabolism. However, these factors were not considere in the present study. Horst and Jorgensen [3] reported a significantly higher plasma cortisol concentration and significantly lower plasma Ca and Pi concentrations in paretic cows. They also described decreased Pi concentrations after cortisol injection in goats. Goff et al [2] observed increases
in plasma cortisol and glucose concentrations and decreased Pi and unchanged Ca concentrations in mastectomized parturient cows. Both studies suggested that the decrease in the plasma Pi concentration was caused by cortisol either directly or indirectly [2,3]. In the present study, we confirmed this suggestion by observing hypophosphatemia in ACTH-infused cows, indicating that the homeostatic mechanism for Pi is different from that for Ca and may be disrupted by the stress response associated with parturition without involvement of gonadal steroid hormones. However, it is difficult to elucidate the hypophosphatemic mechanism in ACTH-infused cows based only on the data presented here. The inhibitory effects of glucocorticoids on renal Pi reabsorption may be the primary cause of hypophosphatemia in ACTH-infused cows. Renal Pi reabsorption is mediated by sodium gradient– dependent phosphate transport (Na-Pi cotransport) and glucocorticoid reduced Na-Pi cotransport mRNA and protein abundance in rats [5,12]. Insulin can also affect Pi homeostasis following ACTH infusion. Increased plasma glucose concentrations after ACTH infusion would be concomitant with increased insulin secretion, which stimulates the flux of Pi into skeletal muscle and induces a decrease in plasma Pi concentration in hu-mans