Receptors for bradykinin and prostaglandin E-2 coupled to Ca2+ signalling in rat cortical collecting duct

In freshly isolated rat cortical collecting ducts (CCD) we measured intracellular Ca2+ activity ([Ca2+](i)) with the Fura-2 method, Bradykinin (BK) induced a transient and biphasic increase in [Ca2+](i). This increase was concentration dependent and was half maximal at a concentration of 15 nM. The B-2 receptor antagonist HOE 140 (100 nM, n = 6) completely abolished BK (100 nM) induced increase in [Ca2+](i). The B-1 receptor agonist des-Arg(9)-bradykinin (100 nM, n = 4) had no effect on [Ca2+](i). In the absence of extracellular Ca2+, the maximal increase in [Ca2+](i) induced by BK was diminished and the secondary plateau phase was completely abolished. Prostaglandin E-2 (PGE(2)) elevated [Ca2+](i) also concentration-dependently and biphasically. A half maximal effect was reached with 1 nM PGE(2). The secondary plateau phase was absent when extracellular Ca2+ was removed. Sulprostone (100 nM, n = 6) mimicked the PGE(2) (100 nM) induced increase in [Ca2+](i). The effect of BK (100 nM) on [Ca2+](i) was not inhibited by the cyclooxygenase inhibitor indomethacin (10 mu M, n = 5). Dopamine (1 mu M, n = 4) did not significantly alter [Ca2+](i). BK and PGE(2) regulate [Ca2+](i) in the rat CCD via release of Ca2+ from intracellular Ca2+ stores as well as via Ca2+ influx from extracellular space. BK directly modulates [Ca2+], through B-2 receptors. EP1 receptors are most likely to be responsible for the PGE(2) induced increase in [Ca2+](i).