Accumulation of intracellular chloride by (Na-K-Cl) co-transport in rat arterial smooth muscle is enhanced in deoxycorticosterone acetate (DOCA)/salt hypertension.

Abstract The accumulation of intracellular chloride above equilibrium by (Na-K-Cl) co-transport has been demonstrated in a variety of tissues [ 1 ], most recently in guinea-pig vas deferens [ 2 ]. The depolarizing influence of the co-transporter on the membrane potential of arterial smooth muscle cells has been demonstrated in rat femoral artery [ 3 ]. The inference is that the depolarisation of membrane potential seen in deoxycorticosterone acetate (DOCA)/salt hypertension is the result of increased chloride accumulation via (Na-K-Cl) co-transport, which is enhanced in hypertension [ 4 ]. The questions addressed here are (i) whether chloride is accumulated above equilibrium in saphenous arterial smooth muscle cells from normotensive animals, and (ii) whether the accumulation is more pronounced in association with DOCA/salt hypertension. In arterial smooth muscle from DOCA/salt hypertensive animals, [Cl] i was significantly elevated ( P 9 ) in comparison to arterial smooth muscle from normotensive control animals. The loop diuretic bumetanide caused a reversible hyperpolarization of E m and a fall in [Cl] i and these effects were enhanced in hypertension. These results are consistent with an increase in the activity of the (Na-K-Cl) co-transporter in rat femoral arterial smooth muscle in DOCA/salt hypertension. A preliminary report of this work has been published [ 5 ].