Endothelium‐derived relaxing factor inhibits the endothelin‐1‐induced increase in protein kinase C activity in rat aorta

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Abstract
1 Particulate and cytosolic protein kinase C (PKC) activity was measured in rat aortae with and without endothelium, following exposure to endothelin-1 (10−8m) 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 (10−6m) or atrial natriuretic peptide (10−6m) and, in endothelium-intact preparations with the calcium ionophore A23187 (10−6m), 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-NG-nitro arginine (5 × 10−5m). 4 These results indicate that EDRF acting via cyclic GMP can inhibit the activation of PKC induced by endothelin-1 in rat aorta.

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