Effects of vasopressin and urea on Ca2+-calmodulin-dependent renal prostaglandin E

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Abstract
Vasopressin (AVP) stimulated immunoreactive prostaglandin E (iPGE) synthesis and the release of [3H]arachidonate (AA) from prelabeled slices of rat inner medulla (IM) in the presence but not in the absence of Ca2+ (plus 2 mM EGTA [ethylene glycol-bis (.beta.-amino ethylether) N,N,N'',N''-tetraacetic acid]). Urea (700-1,200 mosM) inhibited these actions of AVP. By contrast Ca2+ deprivation or urea did not suppress AVP-induced increases in cAMP or stimulation of iPGE by exogenous AA. At 10-50 .mu.M, trifluoperazine (TFP) suppressed AVP-induced increases in [3H]AA release and iPGE accumulation, but not increases in cAMP. Basal acyl hydrolase activity (AH) of 2,000 g particulate fractions of IM was suppressed by EGTA. Ca2+, but not Mg2+ or AVP, restored AH to levels observed in the absence of EGTA. Ca2+-induced increases in particulate AH were inhibited by urea (700-1,200 mosM) or TFP (10-50 .mu.M), but not 1,000 mosM NaCl. Partial depletion of particulate calmodulin-like activity suppressed Ca2+-induced increases in AH. The latter was restored with 1 .mu.M purified exogenous calmodulin but not troponin C. AVP stimulation of AA and PGE release in IM are Ca2+-dependent processes suppressed by urea. A role for Ca2+-calmodulin-dependent AH in the control of PG synthesis in IM is also suggested.