Receptors for bradykinin and prostaglandin E2 coupled to Ca2+ signalling in rat cortical collecting duct.

In freshly isolated rat cortical collecting ducts (CCD) we measured intracellular Ca2+ activity ([Ca2+]j) with the Fura-2 method. Bradykinin (BK) induced a transient and biphasic increase in [Ca2+]j. This increase was concentration dependent and was half maximal at a concentration of 15 nM. The B2 receptor antagonist HOE 140 (100 nM, n = 6) completely abolished BK (100 nM) induced increase in [Ca2+]j. The B1 receptor agonist des-Arg9-bradykinin (100 nM, n = 4) had no effect on [Ca2+]j. In the absence of extracellular Ca2+, the maximal increase in [Ca2+]j, induced by BK was diminished and the secondary plateau phase was completely abolished. Prostaglandin E2 (PGE2) elevated [Ca2+]j, also concentration-dependently and biphasically. A half maximal effect was reached with 1 nM PGE2. The secondary plateau phase was absent when extracellular Ca2+ was removed. Sulprostone (100 nM, n = 6) mimicked the PGE2 (100 nM) induced increase in [Ca2+]j. The effect of BK (100 nM) on [Ca2+]j was not inhibited by the cyclooxygenase inhibitor indomethacin (10 microM, n = 5). Dopamine (1 microM, n = 4) did not significantly alter [Ca2+]j. BK and PGE2 regulate [Ca2+]j 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+]j, through B2 receptors. EP1 receptors are most likely to be responsible for the PGE2 induced increase in [Ca2+]j.