Progesterone Triggers Rapid Transmembrane Calcium Influx And/or Calcium Mobilization from Endoplasmic Reticulum, Via a Pertussis-Insensitive G-protein in Granulosa Cells in Relation to Luteinization Process.

We investigated the early effects (5–60 s) of progesterone (1 pM–0.1 μM) on cytosolic free calcium concentration ([Ca2+]i) and inositol 1,4,5‐trisphosphate (InsP3) formation in nonluteinized and in vitro luteinized porcine granulosa cells (pGCs). Progesterone increased [Ca2+]i and InsP3 formation within 5 s in both cell types. Progesterone induced calcium mobilization from the endoplasmic reticulum via the activation of a phospholipase C linked to a pertussis‐insensitive G‐protein. This process was controlled by protein kinases C and A. In contrast, only nonluteinized pGCs showed a Ca2+ influx via dihydropyridine‐insensitive calcium channel. In both cell types, the nuclear progesterone receptor antagonist RU‐38486 did not inhibit the progesterone‐induced increase in [Ca2+]i; progesterone immobilized on bovine serum albumin, which did not enter the cell, increased [Ca2+]i within 5 s and was a full agonist, but less potent than the free progesterone; pertussis toxin did not inhibit progesterone effect on InsP3. In conclusion, progesterone may interact with membrane unconventional receptors that belong to the class of membrane receptors coupled to a phospholipase C via a pertussis toxin‐insensitive G‐protein. The source of the Ca2+ for the progesterone‐induced increase in [Ca2+]i also depends on the stage of cell luteinization. © 1996 Wiley‐Liss, Inc.