Kallikrein-kinin,enkephalin, renin-aldosterone and catecholamine systems in the vanadate (as vanadyl)-induced arterial hypertension.

Exposure to vanadate was found to induce arterial hypertension through effects on renin-angiotensin-aldosterone, renal peptidergic, and central and peripheral catecholaminergic systems. Vanadate increased, mainly in vascular myocells, both receptor-operated Ca2+ channel- and cyclic-AMP-dependent availability of Ca2+ for contractile processes. Vanadate was selectively accumulated by tissues in the +4 oxidation state (vanadyl).