Factors regulating prostaglandin E2 biosynthesis in renal cortical tubular cells.
Prostaglandin synthesis by isolated rat renal cortical tubular cells was studied in vitro with a superfusion system. The cells were introduced in Teflon chambers and intermittently stimulated. The PGE2 production was measured in the effluent. ANG II (10(-10)-10(-6)M) induced a dose-dependent increase in PGE2 synthesis. Saralasin antagonized the response to ANG II. Hyperosmolar mannitol or NaCl and Ca2+-ionophore A23187 also stimulated PGE2 synthesis. The PGE2 response to all stimuli was blocked in Ca2+-free media containing EGTA. The Ca2+-channel blocker nifedipine (10(-10)-10(-6)M) did not significantly inhibit the PGE2 response to ANG II, hyperosmolar mannitol or NaCl, and A23187, whereas the phospholipase-inhibitors p-bromophenacyl bromide (10(-4)M) and chloroquine (10(-4)M) inhibited the response. Thus, PGE2 synthesis in response to these stimuli in rat renal cortical tubular cell is a Ca2+-dependent process, acting via phospholipases by a mechanism which does not appear to involve voltage-dependent Ca2+-channels.
D000098:Acetophenones / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002738:Chloroquine / Q000494:pharmacology; D015232:Dinoprostone; D005260:Female; D006982:Hypertonic Solutions / Q000494:pharmacology; D007687:Kidney Tubules, Proximal / Q000187:drug effects / Q000378:metabolism*; D008353:Mannitol / Q000494:pharmacology; D010741:Phospholipases A / Q000037:antagonists & inhibitors; D011458:Prostaglandins E / Q000096:biosynthesis*; D051381:Rats; D011919:Rats, Inbred Strains; D012462:Saline Solution, Hypertonic / Q000494:pharmacology
D000098:Acetophenones; D006982:Hypertonic Solutions; D011458:Prostaglandins E; D012462:Saline Solution, Hypertonic; D000804:Angiotensin II; D000001:Calcimycin; D008353:Mannitol; D002738:Chloroquine; D010741:Phospholipases A; D015232:Dinoprostone; C006821:4-bromophenacyl bromide