Enhancement of vascular action of arginine vasopressin by diminished extracellular sodium concentration

Enhancement of vascular action of arginine vasopressin by diminished extracellular sodium concentration. The present study was undertaken to examine the effects of diminished extracellular sodium concentration on the vascular action of arginine vasopressin (AVP) in cultured rat vascular smooth muscle cells (VSMC). The preincubation of cells with the 110 mM extracellular Na + ([Na + ] e ) solution supplemented with 30 mM choline chloride for 60 minutes enhanced the effect of AVP- (1 × 10 -8 M) induced VSMC contraction. The treatment of 110 mM [Na + ] e solution also enhanced the cellular contractile response to the protein kinase C (PKC) activators, phorbol 12-myristate 13-acetate and 1-oleoyl-2-acetyl-glycerol. Furthermore, preincubation with the 110 mM [Na + ] e solution also potentiated the effect of 1 × 10 -8 M AVP, but not 1 × 10 -6 M, to increase the cytosolic-free Ca 2+ ([Ca 2+ ] i ) concentration. The 110 mM [Na + ] e media decreased the basal intracellular Na + concentration and increased intracellular 45 Ca 2+ accumulation, basal [Ca 2+ ] i and AVP-produced 45 Ca 2+ efflux. These effects of 110 mM [Na + ] e solution to enhance the vascular action of AVP were abolished by using Ca 2+ -free 110 mM [Na + ] e solution during the preincubation period. The preincubation with the 110 mM [Na + ] e solution did not change either the K d and B max of AVP V 1 receptor of VSMC or the AVP-induced production of inositol 1,4,5-trisphosphate. The present in vitro results therefore indicate that the diminished extracellular fluid sodium concentration within a range observed in clinical hyponatremic states enhances the vascular action of AVP. The mechanism of this effect appears to be mediated by a potentiation of the AVP-induced increase in [Ca 2+ ] i and enhanced activity of PKC secondary to an increase in the cellular Ca 2+ uptake.