Martín de Aguilera E, Vila J M, Irurzun A, Martínez M C, Martínez Cuesta M A, Lluch S
Departamento de Fisiología, Universidad de Valencia, Spain.
Stroke. 1990 Dec;21(12):1689-93. doi: 10.1161/01.str.21.12.1689.
We studied the effects of vasopressin in isolated segments from branches (500-700 micrograms in external diameter) of human middle cerebral arteries obtained during autopsy of 15 patients who had died 3-8 hours before. Paired segments, one normal and the other de-endothelized by gentle rubbing, were mounted for isometric recording of tension in organ baths. In 11 normal segments, vasopressin produced concentration-dependent contractions with an EC50 of 7.0 X 10(-10) M. Removal of the endothelium from 12 segments did not significantly affect vasopressin-induced contractions. Vasopressin produced further contractions in arterial segments with (n = 4) or without (n = 5) endothelium precontracted with KCl. In segments precontracted with prostaglandin F2 alpha, acetylcholine choline caused relaxation only of those with endothelium. At 10(-8) M (n = 11), the vasopressin V-1 receptor antagonist d(CH2)5Tyr(Me)AVP produced a 60-fold shift to the right of the control response curve for vasopressin. Increasing the concentration of the receptor antagonist to 10(-6) M (n = 7) further displaced the control curve in a parallel manner. These results indicate that vasopressin exerts a powerful constrictor action on isolated human cerebral arteries by direct stimulation of V-1 receptors located predominantly on smooth muscle cells. It appears that this contractile response is not modulated by the presence of an intact endothelial cell layer.
我们研究了血管加压素对15例死亡3至8小时的患者尸检时获取的大脑中动脉分支(外径500 - 700微克)离体节段的作用。将配对节段,一个正常,另一个通过轻柔摩擦去除内皮,安装在器官浴槽中进行张力的等长记录。在11个正常节段中,血管加压素产生浓度依赖性收缩,EC50为7.0×10⁻¹⁰ M。12个节段去除内皮后,血管加压素诱导的收缩无显著影响。血管加压素在预先用氯化钾预收缩的有内皮(n = 4)或无内皮(n = 5)的动脉节段中产生进一步收缩。在预先用前列腺素F2α预收缩的节段中,乙酰胆碱仅使有内皮的节段舒张。在10⁻⁸ M(n = 11)时,血管加压素V - 1受体拮抗剂d(CH2)5Tyr(Me)AVP使血管加压素的对照反应曲线右移60倍。将受体拮抗剂浓度增加到10⁻⁶ M(n = 7)进一步以平行方式使对照曲线移位。这些结果表明,血管加压素通过直接刺激主要位于平滑肌细胞上的V - 1受体,对离体的人脑动脉发挥强大的收缩作用。看来这种收缩反应不受完整内皮细胞层的调节。