Effects of vanadate on vascular smooth muscles of WKY and SHRSP

The effects of vanadate on the vascular smooth muscle of Wistar Kyoto rats (WKY) and stroke prone spontaneously hypertensive rats (SHRSP) were examined. It was shown that sodium vanadate caused contraction of the aortae, mesenteric and basilar arteries of both strains, and that the reactivity was higher in SHRSP in the aorta and mesenteric artery. The vanadate-induced contractions were not blocked by 6-hydroxydopamine, adrenergic blocking agents, indomethacin or ouabain, while 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene did. An increase in K+-concentration potentiated the vanadate-induced contractions of the mesenteric arteries and minimized the difference between preparations from WKY and SHRSP. In depolarized preparations incubated in K-Tyrode's solution (140 mM KCl), vanadate induced phasic contractions followed by marked relaxation in the aortae of both species, the relaxation being more prominent in SHRSP aorta, while depolarized mesenteric arteries showed sustained contractions. It was revealed that vanadate caused contractions by acting inside the cell, and membrane permeability to vanadate might be higher in the vascular smooth muscle of SHRSP. The findings also suggested that vanadium, an inorganic element, can be involved in the initiation of hypertension in SHRSP when it acts on vascular smooth muscle.