SALT LOADS ATTENUATE POTASSIUM-INDUCED VASODILATION OF FOREARM VASCULATURE IN HUMANS

To evaluate the role of the sodium pump in resistance control in vivo, we studied vascular responses to potassium, which produces vasodilation by the activation of vascular Na+,K+-ATPase, in normotensive volunteers receiving a high salt diet compared with volume-depleted subjects receiving diuretic treatment. Forearm blood flow was measured by strain-gauge plethysmography during small increments in local concentrations of potassium with intrabrachial arterial infusions of KCl. Infusions of 0.12 and 0.24 mEq/min KCl increased forearm blood flow and decreased forearm vascular resistance in a dose-dependent fashion. But the simultaneous intrabrachial arterial infusion of 2 mug/min ouabain, a Na+,K+-ATPase inhibitor, could blunt the decremental response of vascular resistance to 0.12 mEq/min KCl. The decrements of vascular resistance with KCl infusions divided by the initial resistance were significantly less with ouabain compared with those without ouabain (43+/-4% versus 57+/-3%, p<0.01). This suggests that potassium produces vasodilation by the activation of vascular Na+,K+-ATPase activity. Similarly, salt loading (180 mEq NaCl for 7 days) after treatment with diuretics could attenuate percent decrements of resistance with KCl infusions (39+/-3% versus 53+/-2%, p<0.01), whereas vascular resistance responses to sodium nitroprusside, a nonspecific vasodilator, and to verapamil, a calcium antagonist, did not change with salt loading after volume depletion. Therefore, salt loading could attenuate forearm vascular response to potassium specifically, as did the administration of ouabain. Evidence supports the hypothesis that volume expansion with salt loading increases endogenous ouabainlike Na+,K+-ATPase inhibitor concentration, which plays a role in not only the control of extracellular fluid but also the regulation of vascular tone during salt loading.