Arginine vasopressin enhances sympathetic constriction through the V1 vasopressin receptor in human saphenous vein.
Arginine vasopressin enhances sympathetic constriction through the V1 vasopressin receptor in human saphenous vein.
复制标题
精氨酸加压素通过人隐静脉中的 V1 加压素受体增强交感神经收缩。
作者：
P. Medina;A. Acuña;J. Martínez;E. Otero;J. Vila;M. Aldasoro;S. Lluch
背景
精氨酸加压素（AVP）不仅通过刺激V1受体直接作用于血管，而且在动物体内和体外实验中也可调节肾上腺素能介导的反应。本研究的目的是探讨是否AVP可以促进异常肾上腺素能收缩反应的人隐静脉。
方法和结果
隐静脉环取自32例接受冠状动脉搭桥手术的患者。将静脉环悬挂在器官浴室中用于张力的等长记录。AVP（3 × 10 ~（-9）mol/L）可增强1、2和4 Hz电场刺激引起的收缩（分别增强80%、70%和60%），并使去甲肾上腺素的浓度-反应曲线发生明显偏移（半数有效浓度从6.87 × 10 ~（-7）mol/L降至1.04 × 10 ~（-7）mol/L; P<0.05）。V1受体拮抗剂d（CH 2）5 Tyr（Me）AVP（10[-6] mol/L）可阻断AVP引起的增强作用。选择性V1受体激动剂[Phe，2 Orn 8]-vasotocin（3 × [-10]-9 mol/L）可增强电刺激诱发的反应，V1受体拮抗剂（10[-6] mol/L）也可抑制该反应。相反，V2受体激动剂去氨加压素（10[-9]~ 10[-7] mol/L）不能改变神经原性反应，V2受体拮抗剂[d（CH 2）5，D-Ile，2 Ile，4 Arg 8]-加压素（10[-8]~ 10[-6] mol/L）不能阻止AVP引起的增强作用。二氢吡啶类钙拮抗剂硝苯地平（10[-6] mol/L）不影响AVP的增强作用。
结论
结果提示，低浓度AVP促进交感神经传递，增强去甲肾上腺素对人隐静脉的收缩作用。这些作用似乎是由V1受体刺激介导的，并且不依赖于通过二氢吡啶钙通道的钙进入。因此，AVP可能有助于与静脉移植物相关的急性缺血综合征的血管机制，特别是如果交感神经系统被激活。
BACKGROUND
Arginine vasopressin (AVP) not only acts directly on blood vessels through V1 receptor stimulation but also may modulate adrenergic-mediated responses in animal experiments in vivo and in vitro. The aim of the present study was to investigate whether AVP can contribute to an abnormal adrenergic constrictor response of human saphenous veins.
METHODS AND RESULTS
Saphenous vein rings were obtained from 32 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. AVP (3x10[-9] mol/L) enhanced the contractions elicited by electrical field stimulation at 1, 2, and 4 Hz (by 80%, 70%, and 60%, respectively) and produced a leftward shift of the concentration-response curve to norepinephrine (half-maximal effective concentration decreased from 6.87x10[-7] to 1.04x10[-7] mol/L; P<.05). The V1 vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP (10[-6] mol/L) prevented the potentiation evoked by AVP. The selective V1 receptor agonist [Phe,2 Orn8]-vasotocin (3x[-10]-9 mol/L) induced potentiation of electrical stimulation-evoked responses, which was also inhibited in the presence of the V1 receptor antagonist (10[-6] mol/L). In contrast, the V2 receptor agonist desmopressin (10[-9] to 10[-7] mol/L) did not modify neurogenic responses, and the V2 receptor antagonist [d(CH2)5, D-Ile,2 Ile,4 Arg8]-vasopressin (10[-8] to 10[-6] mol/L) did not prevent the potentiation induced by AVP. The dihydropyridine calcium antagonist nifedipine (10[-6] mol/L) did not affect the potentiating effect of AVP.
CONCLUSIONS
The results suggest that low concentrations of AVP facilitate sympathetic neurotransmission and potentiate constrictor effects of norepinephrine in human saphenous veins. These effects appear to be mediated by V1 receptor stimulation and are independent of calcium entry through dihydropyridine calcium channels. Thus, AVP may contribute to vascular mechanisms involved in acute ischemic syndromes associated with venous grafts, particularly if the sympathetic nervous system is activated.
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