Barium reduces resting blood flow and inhibits potassium-induced vasodilation in the human forearm.

Increasing extracellular K+ concentration within and just above the physiological range hyperpolarizes and relaxes vascular smooth muscle in vitro. These actions involve inwardly rectifying potassium channels (K(IR)) and Na+/K+ ATPase, which are inhibited, respectively, by Ba2+ and ouabain. The role (if any) of K(IR) in controlling human resistance vessel tone is unknown, and we investigated this in the forearm. Blood flow was measured by plethysmography in healthy men. Drugs and electrolytes were infused through the brachial artery. BaCl2 (4 micromol/min, also used in subsequent experiments) increased Ba2+ plasma concentration in the infused forearm to 50+/-0.8 micromol/L (mean+/-SEM) and reduced blood flow by 24+/-4% (n=8, P<0.001) without causing systemic effects. Ouabain (2.7 nmol/min), alone and with BaCl2, reduced flow by 10+/-2% and 28+/-3%, respectively (n=10). Incremental infusions of KCl (0.05, 0.1, and 0.2 mmol/min) increased flow from baseline by 1.0+/-0.2, 2.0+/-0.4, and 4.2+/-0.5 mL/min per deciliter forearm, respectively. Responses to KCl (0.2 mmol/min) were inhibited by BaCl2, alone and plus ouabain, by 60+/-9% and 88+/-6%, respectively (both P< or =0.01). In control experiments, norepinephrine (240 pmol/min) reduced blood flow by 24+/-2% but had no significant effect on K+-induced vasodilation. BaCl2, alone or with ouabain, did not significantly influence responses to verapamil or nitroprusside. Ba2+ increases forearm vascular resistance. K+-induced vasodilation is selectively inhibited by Ba2+ and almost abolished by Ba2+ plus ouabain, suggesting a role for K(IR) and Na+/K+ ATPase in controlling basal tone and in K+-induced vasorelaxation in human forearm resistance vessels.