REDUCED CYTOSOLIC-FREE SODIUM CONCENTRATION IN VASCULAR SMOOTH-MUSCLECELLS FROM SPONTANEOUSLY HYPERTENSIVE RATS

1. Cytosolic free sodium concentration and sodium transport systems we re measured in Intact cultured vascular smooth muscle cells from spont aneously hypertensive rats of the Munster strain and from normotensive Wistar-Kyoto rats using the sodium-sensitive fluorescent dye sodium-b inding benzofuran isophthalate. 2. Resting cytosolic free sodium conce ntration 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. Inhibiti on of Na+, K+-ATPase by ouabain caused a dose-dependent increase in cy tosolic free sodium concentration in spontaneously hypertensive rats a nd Wistar-Kyoto rats. 4. Activation of Na+-Ca2+ exchange by lonomycin increased cytosolic free sodium concentration in both strains. However , the ionomycin-induced increase In cytosolic free sodium concentratio ns was significantly higher In vascular smooth muscle cells from spont aneously hypertensive rats than from Wistar-Kyoto rats (220+/-35% of t he resting cytosolic free sodium concentration versus 148+/-27%; P<0.0 5). The ionomycin-induced Increase in cytosolic free sodium concentrat ion was prevented in the absence of external sodium or by inhibition o f Na+-Ca2+ exchange by NICl2. 5. Activation of Na+-H+ exchange by intr acellular 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 c oncerning the role of cytosolic free sodium concentration In the patho genesis of primary hypertension need to be reinvestigated. However, th e conclusions from results obtained In cultured vascular smooth muscle cells are limited with respect to conditions in vivo.