The role of the sodium-calcium (Na-Ca) exchange in vascular smooth muscle contraction was examined in tail artery rings isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and in normotensive Wistar-Kyoto rats (WKY). The rings were repeatedly stimulated with noradrenaline (1 microM) in physiological salt solution (Na = 130 mM), until two successive contractions were of the same magnitude. The rings were then placed in physiological salt solution with reduced sodium concentrations (65 mM or 0 mM, replaced isosmotically with sucrose), and the noradrenaline stimulations continued. In WKY rings, the reduction of sodium concentration produced an increase in the response to noradrenaline, which was significant in sodium-free physiological salt solution. In SHRSP rings, however, the same reductions in sodium concentration produced significantly less potentiation of the noradrenaline contraction, even in sodium-free physiological salt solution. We conclude that (1) in WKY, the reduced and reversed activity of the Na-Ca exchange produced by the reductions in sodium concentration makes more calcium available for contraction when the smooth muscle is stimulated with noradrenaline; and (2) the failure of sodium reductions to produce a normal potentiation of the response to noradrenaline in SHRSP indicates a depressed activity of the Na-Ca exchange in this tissue.