Actions of vanadate on vascular tension and sodium pump activity in cat isolated cerebral and femoral arteries

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Abstract
The mechanisms involved in the responses induced by sodium vanadate (Va3 VO4) on cat cerebral and femoral arteries were studied. The possibility that these responses were due to Na+, K+‐ATPase inhibition was investigated by measuring the effect of vanadate on [3H]‐ouabain binding to arterial membrane fractions, K+‐induced vasodilatation and ouabain‐sensitive 86Rb+ uptake. The vanadium compounds (Na3VO4, VOSO4, VCl3 and O5V3) induced similar, concentration‐dependent contractions in each kind of artery, the cerebral vessels being the most sensitive to these compounds. Exposure of the arteries to a low‐Na+ (25 mm) solution suppressed the contraction caused by vanadate in femoral but not in cerebral arteries. Vanadate‐induced contractions were reduced in Ca2+‐free medium but remained unaffected by 3 × 10−6 m phentolamine, reserpine pretreatment or 3 × 10−6 m verapamil in both kinds of artery. The addition of 7.5 mm K+ to the arteries immersed in a K+‐free solution induced vasodilatation, which was not modified by 10−3 m vanadate. The consecutive administration of ouabain (10−4 m) and vanadate (10−3 m) (or vice versa), or the simultaneous administration of both agents (10−8 to 10−3 m) appeared to produce an additive contraction in both types of artery. Vanadate (10−7 to 10−3 m) did not displace the [3H]‐ouabain binding to arterial membrane fractions of these arteries, whereas 10−4 m ouabain did. In both kinds of artery, total 86Rb+ uptake was reduced by ouabain (10−8 to 10−3 m), in a concentration‐dependent manner, whereas it was not modified by vanadate (10−8‐10−3 m). These results suggest that vanadate induces contraction in both types of artery by a mechanism unrelated to Na+, K+‐ATPase inhibition. Such a mechanism is likely to be related to inhibition of the Ca2+‐ATPase of the cell membrane and/or the sarcoplasmic reticulum.