Abstract
The effect of osmolality variations on the membrane permeability of vascular smooth muscle to sodium and potassium was investigated by studying the washout of 24Na and 41K at different extracellular tonicities. The K efflux in normal Krebs was 4.1 10‐12 M/cm2 sec at 37° C and 2.0 10‐12 M/cm2 sec at 15° C. The corresponding Pk values were 9.4 10‐8 and 5.3 10‐8 cm/sec, respectively, assuming a membrane potential of 50 mV at 37° C and 40 mV at 15° C.A substantial fraction of the sodium content of the portal vein prevails in an osmotically inactive bound form, as demonstrated in uptake studies on preparations where cell membranes had been destroyed so as to give a homogenous tissue fluid phase (Haljamäe et al. 1970). The present 24Na washout experiments performed on “normal” portal vein tissues were for this reason completed with studies of 24Na efflux from such damaged veins. Evidence is presented for the existence of one intra‐cellular and one extracellular fraction of bound sodium. Subtraction of that component in the washout curve which represented the intracellularly bound Na fraction would yield the exchange kinetics of the “free” intracellular sodium. The magnitude and efflux of [Na+]1, thus calculated, amounted to 13.1 meq/l and 1.2 10‐12 M/cm2 sec at 15° C.Assuming, on the basis of indirect experimental evidence, that Na influx equals Na efflux in the experimental situation, a passive permeability coefficient for Na of 4.3 10‐9 cm/sec was calculated, giving a Pna/Pk ratio of 0.081. The washout experiments performed in anisosmotic media indicated that this ratio increased when osmolality was lowered, which might in part explain the strong enhancement of the spontaneous activity induced by hypotonicity. The results did not, however, indicate any clearcut alteration in either Pna, or Pk when the muscle cells were exposed to hypertonicity.