Calcium-dependent modulation of guanosine 3',5'-monophosphate in renal cortex. Possible relationship to calcium-dependent release of fatty acid.
Calcium-dependent modulation of guanosine 3',5'-monophosphate in renal cortex. Possible relationship to calcium-dependent release of fatty acid.
复制标题
肾皮质中鸟苷 3,5-单磷酸的钙依赖性调节。
DOI：
10.1016/0006-2952(80)90546-8
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发表时间：
1980
影响因子：
5.8
通讯作者：
Derubertis,FR
中科院分区：
文献类型：
--
作者：
Briggs,RG;Derubertis,FR
The effects of Ca2+on cGMP accumulation in rat renal cortical slices were correlated with the effects on14C-fatty acid release in tissue prelabeled with14C arachidonate. Ca2+in the presence and absence of ionophore A23187 exerted parallel effects on the release of labeled arachidonate from slices and on slice cGMP content. Thus, Ca2+stimulated both arachidonate release and tissue cGMP accumulation 2 to 3-fold when added to slices of renal cortex previously deprived of Ca2+and Mg2+, whereas Mg2+had no stimulatory effect on either arachidonate release or tissue cGMP content. In the presence of A23187, Ca2+increased arachidonate release and tissue cGMP accumulation 4 to 6-fold. Tetracaine partially inhibited Ca2+-induced arachidonate release and completely blocked Ca2+-induced cGMP accumulation. Ca2+-induced arachidonate release was unaffected by the absence of O2. Addition of exogenous arachidonate to slices of renal cortex increased tissue cGMP content 2-fold. Linoleate exerted a lesser effect on tissue cGMP, while palmitate and oleate had no effect. Ca2+- and arachidonateinduced cGMP contents in renal cortical slices were not additive, and both were abolished by exclusion of O2. Since nitroprusside increased cGMP accumulation 10- to 15-fold in O2-deprived slices, loss of the Ca2+and arachidonate responses under these incubation conditions was selective. Ca2+-induced cGMP accumulation was unaffected by indomethacin (100 μg/ml), but was abolished by 200 μM 5,8,11,14-eicosatetraynoic acid (TYA). The results are consistent with the possibility that the Ca2+-dependent processes regulating cGMP in renal cortex include Ca2+-dependent acyl hydrolase activity, which limits the availability of free polyunsaturated fatty acids. A role for fatty acid oxygenation products in the stimulation of cGMP is suggested, but not established, by the O2dependence of the actions of both Ca2+and exogenous fatty acids. The failure of exogenous arachidonate or linoleate to mimic quantitatively the actions of Ca2+on cGMP may reflect the involvement of other Ca2+- and O2-dependent processes in modulation of cGMP in this tissue or limited access of exogenous fatty acid to cGMP regulatory sites in the cell.
