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Endothelium‐derived relaxing factor inhibits the endothelin‐1‐induced increase in protein kinase C activity in rat aorta
Author(s) -
Lang D.,
Lewis M.J.
Publication year - 1991
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1991.tb12398.x
Subject(s) - protein kinase c , endothelium , endothelium derived relaxing factor , endocrinology , sodium nitroprusside , endothelin receptor , medicine , endothelin 1 , nitric oxide , chemistry , atrial natriuretic peptide , cytosol , endothelins , cyclic guanosine monophosphate , biology , kinase , biochemistry , enzyme , receptor
1 Particulate and cytosolic protein kinase C (PKC) activity was measured in rat aortae with and without endothelium, following exposure to endothelin‐1 (10 −8 m ) for various time intervals. 2 Endothelin‐1 induced two peaks of particulate PKC activity, occurring at 30s and 10 min exposure times in both endothelium‐intact and endothelium‐denuded preparations. Cytosolic PKC activity fell below baseline at all incubation times studied. 3 In endothelium‐denuded preparations, elevation of guanosine 3′:5′‐cyclic monophosphate (cyclic GMP) levels with sodium nitroprusside (10 −6 m ) or atrial natriuretic peptide (10 −6 m ) and, in endothelium‐intact preparations with the calcium ionophore A23187 (10 −6 m ), inhibited the activation of particulate PKC activity seen after incubation with endothelin‐1 for 30 s. The inhibitory effect of A23187 was prevented by prior incubation of the endothelium‐intact vessels with the nitric oxide synthetase inhibitor, l ‐N G ‐nitro arginine (5 × 10 −5 m ). 4 These results indicate that EDRF acting via cyclic GMP can inhibit the activation of PKC induced by endothelin‐1 in rat aorta.