1. Cytosolic free sodium concentration and sodium transport systems were measured in intact cultured vascular smooth muscle cells from spontaneously hypertensive rats of the Münster strain and from normotensive Wistar-Kyoto rats using the sodium-sensitive fluorescent dye sodium-binding benzofuran isophthalate. 2. Resting cytosolic free sodium concentration was significantly lower in vascular smooth muscle cells from spontaneously hypertensive rats than from Wistar-Kyoto rats (10.2 +/- 1.5 mmol/l, n = 26, versus 19.4 +/- 2.5 mmol/l, n = 20, P < 0.01). 3. Inhibition of Na+, K(+)-ATPase by ouabain caused a dose-dependent increase in cytosolic free sodium concentration in spontaneously hypertensive rats and Wistar-Kyoto rats. 4. Activation of Na(+)-Ca2+ exchange by ionomycin increased cytosolic free sodium concentration in both strains. However, the ionomycin-induced increase in cytosolic free sodium concentrations was significantly higher in vascular smooth muscle cells from spontaneously hypertensive rats than from Wistar-Kyoto rats (220 +/- 35% of the resting cytosolic free sodium concentration versus 148 +/- 27%; P < 0.05). The ionomycin-induced increase in cytosolic free sodium concentration was prevented in the absence of external sodium or by inhibition of Na(+)-Ca2+ exchange by NiCl2. 5. Activation of Na(+)-H+ exchange by intracellular acidification of vascular smooth muscle cells with propionic acid increased cytosolic free sodium concentration in each strain (19.6 +/- 5.7 versus 16.3 +/- 3.2 mmol/l). 6. It is concluded that concepts concerning the role of cytosolic free sodium concentration in the pathogenesis of primary hypertension need to be reinvestigated.(ABSTRACT TRUNCATED AT 250 WORDS)