[Interaction of protein kinase C-extracellular signal-regulated kinase 1/2 signal pathway in the process of plasminogen activator inhibitor-1 expression induced by nicotine in human umbilical vein endothelial cells].

Objective: To explore the role of protein kinase C (PKC)- extracellular signal-regulated kinase (ERK)1/2 signal pathway in the process of plasminogen activator inhibitor-1 (PAI-1) protein and mRNA expression in cultured human umbilical vein endothelial cells (HUVECs) induced by nicotine.

Methods: HUVECs were cultured to examine the effect of nicotine on the expression of secreting PAI-1 in HUVECs on different experimental conditions. The expression of PAI-1 protein was measured by ELISA.

ATP-sensitive potassium channels and endogenous adenosine are involved in spinal antinociception produced by locus coeruleus stimulation.

The effects of locus coeruleus stimulation on nociceptive evoked discharges of thalamic parafascicular (PF) neurons were investigated in lightly urethane-anesthetized rats, aiming to study the mechanisms underlying these effects. Intrathecal (i.t.

ATP-sensitive potassium channels and endogenous adenosine are involved in spinal antinociception produced by locus coeruleus stimulation.

It has been known that locus coeruleus (LC) stimulation suppresses nociceptive discharges of the thalamic parafascicular (PF) neurons through the spinally descending adrenergic terminals which inhibit the transmission of nociceptive signals in the spinal dorsal horn. This experimental model was used in the present study to analyze the detailed processes that happened in the dorsal horn following norepinephrine release by preemptive intrathecal (i.t.