Abstract
The effect of interaction between Ca and prostaglandin (PG) on the action of antidiuretic hormone (ADH) was studied in the water-diuresing anesthetized dog. Maximal urinary osmolality after 100 mU of ADH was 331 .+-. 24 in the normocalcemic state vs. only 228 .+-. 31 mOsmol/kg (P < 0.01) in dogs made acutely hypercalcemic when their serum Ca concentration was increased from 8.9 .+-. 0.2 to 11.6 .+-. 0.4 mg/100 ml (P < 0.001). To define the role of PG in this effect, studies were performed in the presence of PG inhibition with indomethacin (10 mg/kg). The antidiuretic response to 100 mU of ADH was decreased by hypercalcemia, as maximal osmolality was 1096 .+-. 65 in the normocalcemic PG-inhibited dog but only 555 .+-. 50 mOsmol/kg in the acutely hypercalcemic PG-inhibited dog (P < 0.001). Conversely, the effect of PG inhibition to enhance the hydroosmotic effect of ADH was also demonstrable in actuely hypercalcemic dogs, as maximal urinary osmolality following 100 mU of ADH was 257 .+-. 9 before and 557 .+-. 60 mOsmol/kg after PG inhibition (P < 0.001). The effect of acute hypercalcemia on the hydroosmotic response to vasopressin is not dependent on the synthesis of an endoperoxide metabolite. Likewise, hypercalcemia blunts but does not abolish the effect of PG inhibitors to potentiate the hydroosmotic effect of ADH.