Barium Reduces Resting Blood Flow and Inhibits Potassium-Induced Vasodilation in the Human Forearm

Abstract

Background — 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 Ba 2+ and ouabain. The role (if any) of K IR in controlling human resistance vessel tone is unknown, and we investigated this in the forearm. Methods and Results — Blood flow was measured by plethysmography in healthy men. Drugs and electrolytes were infused through the brachial artery. BaCl 2 (4 μmol/min, also used in subsequent experiments) increased Ba 2+ plasma concentration in the infused forearm to 50±0.8 μmol/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 BaCl 2 , 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 BaCl 2 , alone and plus ouabain, by 60±9% and 88±6%, respectively (both P ≤0.01). In control experiments, norepinephrine (240 pmol/min) reduced blood flow by 24±2% but had no significant effect on K + -induced vasodilation. BaCl 2 , alone or with ouabain, did not significantly influence responses to verapamil or nitroprusside. Conclusions — Ba 2+ increases forearm vascular resistance. K + -induced vasodilation is selectively inhibited by Ba 2+ and almost abolished by Ba 2+ 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.