SUMMARY

The effects of a2-adrenergic receptors are usually attributed to inhibition of adenylyl cyclase through pertussis toxin-sensitive G coupling. In kidney distal convoluted tubule (DOT) cells, stimulation of NaVK-ATPase by 02 receptors involves activa-tion of protein kinase C (PKC). To identify the signal pathways coupled to 02 receptors, we measured cAMP production and show that the 02 agonist B-HT 933 had no effect on basal or stimulated (forskolin, parathyroid hormone) cAMP accumula-tion in DCT cells but inhibited parathyroid hormone-stimulated cAMP accumulation in proximal tubule cells. I tested whether 02 receptors on DCT cells stimulate PKC through second mes-sengers generated from phospholipase C (PLC) activation. In DCI cells, B-HT 933 increased inositol-1,4,5-trisphosphate for-mation by 4-6-fold over control and increased diacylglycerol formation by 46%. Basal intracellular calcium concentration i