James G M, Hodgson W C
Department of Pharmacology, Monash University, Clayton, Victoria, Australia.
Eur J Pharmacol. 1997 Mar 12;322(1):55-8. doi: 10.1016/s0014-2999(96)00986-7.
We investigated protein kinase C participation in the contractile response to 5-hydroxytryptamine (5-HT), and in the interaction between 5-HT and endothelin-1, in aortas from control and diabetic rats. Diabetic rats display attenuated reactivity to 5-HT (i.e., approximately 47% of control maximum). The protein kinase C inhibitor calphostin C (1 microM) significantly reduced responses to 5-HT only in aortas from control rats. In diabetic rats, maximum responses to 5-HT, in the presence of endothelin-1 (3 nM), were not significantly different to controls. The additional presence of calphostin C significantly reduced responses only in aortas from diabetic rats. These results may indicate an abnormality in the protein kinase C second messenger system during diabetes.
我们研究了蛋白激酶C在对照大鼠和糖尿病大鼠主动脉中对5-羟色胺（5-HT）的收缩反应以及5-HT与内皮素-1之间相互作用中的参与情况。糖尿病大鼠对5-HT的反应性减弱（即约为对照最大值的47%）。蛋白激酶C抑制剂钙泊三醇C（1微摩尔）仅在对照大鼠的主动脉中显著降低了对5-HT的反应。在糖尿病大鼠中，在内皮素-1（3纳摩尔）存在的情况下，对5-HT的最大反应与对照无显著差异。钙泊三醇C的额外存在仅在糖尿病大鼠的主动脉中显著降低了反应。这些结果可能表明糖尿病期间蛋白激酶C第二信使系统存在异常。
