García-Villalón A L, Padilla J, Monge L, Fernández N, Sánchez M A, Gómez B, Diéguez G
Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Madrid, Spain.
Br J Pharmacol. 1999 Feb;126(3):785-93. doi: 10.1038/sj.bjp.0702345.
In order to analyse the effects of arginine-vasopressin on the vascular contraction to sympathetic nerve stimulation during cooling, the isometric response of isolated, 2-mm segments of the rabbit central ear (cutaneous) artery to electrical field stimulation (1-8 Hz) was recorded at 37 and 30 degrees C. Electrical stimulation (37 degrees C) produced frequency-dependent arterial contraction, which was reduced at 30 degrees C and potentiated by vasopressin (10 pM, 100 pM and 1 nM). This potentiation was greater at 30 than at 37 degrees C and was abolished at both temperatures by the antagonist of vasopressin V1 receptors d(CH2)5 Tyr(Me)AVP (100 nM). Desmopressin (1 microM) did not affect the response to electrical stimulation. At 37 degrees C, the vasopressin-induced potentiation was abolished by the purinoceptor antagonist PPADS (30 microM), increased by phentolamine (1 microM) or prazosin (1 microM) and not modified by yohimbine (1 microM), whilst at 30 degrees C, the potentiation was reduced by phentolamine, yohimbine or PPADS, and was not modified by prazosin. The Ca2+-channel blockers, verapamil (10 microM) and NiCl2 (1 mM), abolished the potentiating effects of vasopressin at 37 degrees C whilst verapamil reduced and NiCl2 abolished this potentiation at 30 degrees C. The inhibitor of nitric oxide synthesis, L-NOARG (100 microM), or endothelium removal did not modify the potentiation by vasopressin at 37 and 30 degrees C. Vasopressin also increased the arterial contraction to the alpha2-adrenoceptor agonist BHT-920 (10 microM) and to ATP (2 mM) at 30 and 37 degrees C, but it did not modify the contraction to noradrenaline (1 microM) at either temperature. These results suggest that in cutaneous (ear) arteries, vasopressin potentiaties sympathetic vasoconstriction to a greater extent at 30 than at 37 degrees C by activating vasopressin V1 receptors and Ca2+ channels at both temperatures. At 37 degrees C, the potentiation appears related to activation of the purinoceptor component and, at 30 degrees C, to activation of both purinoceptor and alpha2-adrenoceptor components of the sympathetic response.
为了分析精氨酸加压素对降温期间交感神经刺激引起的血管收缩的影响，在37℃和30℃下记录了兔中耳（皮肤）动脉2毫米离体节段对电场刺激（1 - 8赫兹）的等长反应。电刺激（37℃）引起频率依赖性动脉收缩，在30℃时收缩减弱，且加压素（10皮摩尔、100皮摩尔和1纳摩尔）可增强收缩。这种增强在30℃时比在37℃时更明显，且在两个温度下均被加压素V1受体拮抗剂d(CH2)5 Tyr(Me)AVP（100纳摩尔）消除。去氨加压素（1微摩尔）不影响对电刺激的反应。在37℃时，嘌呤受体拮抗剂PPADS（30微摩尔）可消除加压素诱导的增强作用，酚妥拉明（1微摩尔）或哌唑嗪（1微摩尔）可增强该作用，而育亨宾（1微摩尔）则无此作用；而在30℃时，酚妥拉明、育亨宾或PPADS可减弱增强作用，哌唑嗪则无此作用。钙通道阻滞剂维拉帕米（10微摩尔）和氯化镍（1毫摩尔）在37℃时可消除加压素的增强作用，维拉帕米在30℃时可减弱该增强作用，氯化镍则可消除该作用。一氧化氮合成抑制剂L - NOARG（100微摩尔）或去除内皮均不改变37℃和30℃时加压素的增强作用。加压素在30℃和37℃时还可增强动脉对α2 - 肾上腺素能受体激动剂BHT - 920（10微摩尔）和ATP（2毫摩尔）的收缩反应，但在任一温度下均不改变对去甲肾上腺素（1微摩尔）的收缩反应。这些结果表明，在皮肤（耳）动脉中，加压素在30℃时比在37℃时通过激活两个温度下的加压素V1受体和钙通道，更大程度地增强交感神经血管收缩。在37℃时，增强作用似乎与嘌呤受体成分的激活有关，而在30℃时，与交感反应中嘌呤受体和α2 - 肾上腺素能受体成分的激活有关。
