钒酸盐及其他钒化合物对大鼠输精管的收缩作用。

Contractile effect of vanadate and other vanadium compounds on the rat vas deferens.

作者信息

Garcia A G, Jurkiewicz A, Jurkiewicz N H

出版信息

Eur J Pharmacol. 1981 Mar 5;70(1):17-23. doi: 10.1016/0014-2999(81)90427-1.

Abstract

Sodium metavanadate (NaVO3), vanadium pentoxide (V2O5) and vanadyl sulphate (VOSO4), evoked rhythmic and tonic contractions of the normal and reserpinized rat isolated vas deferens. Contractions were not observed by the use of vanadium trichloride (VCl3) The order of potency of these compounds, for their maximum contractile effects was NaVO3 greater than V2O5 greater than VOSO4 greater than VCl3. Differences in pD2 values were less than 0.5 long units in relation to the first compound. Vanadium-induced contractions were blocked by Ca2+ deprivation, nifedipine, Mg2+, Mn2+, Ni2+ and Co2+, indicating the involvement of a loosely bound or extracellular calcium-dependent mechanism. It is still unclear whether this calcium translocation was related, or not, to changes in Na+, K+-ATPase activity. Since ouabain blocked the action of vanadyl or vanadate non-competitively, it is concluded that vanadium compounds and ouabain induce their effects by interacting with different sites in vas deferens, both of which may or may not be located on the (Na+, K+)ATPase enzyme complex.

摘要

偏钒酸钠（NaVO₃）、五氧化二钒（V₂O₅）和硫酸氧钒（VOSO₄）可引起正常和利血平化大鼠离体输精管的节律性和强直性收缩。使用三氯化钒（VCl₃）未观察到收缩。这些化合物产生最大收缩效应的效力顺序为NaVO₃＞V₂O₅＞VOSO₄＞VCl₃。相对于第一种化合物，pD2值的差异小于0.5个对数单位。钒诱导的收缩被剥夺Ca²⁺、硝苯地平、Mg²⁺、Mn²⁺、Ni²⁺和Co²⁺所阻断，表明涉及一种松散结合或细胞外钙依赖性机制。目前尚不清楚这种钙转运是否与Na⁺、K⁺-ATP酶活性的变化有关。由于哇巴因非竞争性地阻断硫酸氧钒或钒酸盐的作用，得出的结论是，钒化合物和哇巴因通过与输精管中的不同位点相互作用来诱导其效应，这两个位点可能位于（Na⁺、K⁺）ATP酶复合物上，也可能不在该复合物上。