Koskinen L O
Department of Physiology and Medical Biophysics, University of Uppsala, Sweden.
Acta Physiol Scand. 1994 Dec;152(4):399-406. doi: 10.1111/j.1748-1716.1994.tb09822.x.
TRH has pronounced vascular effects. The final transmitter mechanisms of these effects are not fully understood. The present study was conducted in order to elucidate whether these effects are mediated by prostaglandic or muscarinic mechanisms. Muscarinic blockade augmented the vasoconstricting- and pressor effect of TRH; vasodilation in the brain was attenuated only in the caudate nucleus. Indomethacin provoked a decrease in regional cerebral blood flow and in the gastric mucosal blood flow. No effect of indomethacin was observed on the vascular effects of TRH. It is concluded that the cerebral vasodilating and peripheral vasoconstricting effects of TRH are not mediated by prostaglandins. Muscarinic mechanisms are involved in the vasodilating effect of TRH only in the caudate nucleus.
促甲状腺激素释放激素（TRH）具有显著的血管效应。这些效应的最终递质机制尚未完全明确。开展本研究是为了阐明这些效应是否由前列腺素或毒蕈碱机制介导。毒蕈碱阻断增强了TRH的血管收缩和升压效应；仅在尾状核中，TRH引起的脑内血管舒张作用减弱。吲哚美辛可使局部脑血流量和胃黏膜血流量减少。未观察到吲哚美辛对TRH的血管效应有影响。得出的结论是，TRH的脑血管舒张和外周血管收缩效应并非由前列腺素介导。毒蕈碱机制仅在尾状核中参与TRH的血管舒张效应。
