Effects of Digoxin on Isolated Human Peripheral Arteries and Veins

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Abstract
In isolated human crural arteries and veins, digoxin induced slowly developing, long-lasting contractions. These contractions were not diminished by .alpha.-adrenoceptor blockade or by washing, but were abolished by the Ca antagonist nifedipine. In the presence of digoxin, the maximum contractile responses to noradrenaline [norepinephrine, NA] (18 .mu.M) and K (127 mM) markedly increased, and the glycoside shifted the NA concentration-response curve to the left. Immersion of vein preparations in Ca-free medium for 30 min. abolished the digoxin contraction but responses could still be elicited by K and NA. A change of the extracellular K concentration from 4.6 mM in normal Krebs to 1.15 mM always increased tension in vein preparations, but a change from 4.6-6.9 and 9.2 mM caused relaxation, and a further increase to 13.8 mM contracted the preparations. After pretreatment with digoxin (1 .mu.M), a K change from 4.6-1.15 mM caused relaxation and all concentrations exceeding 4.6 mM produced contraction. Apparently digoxin has a direct contractile effect on isolated human crural vessels, and this effect is dependent on the extracellular Ca concentration. In the presence of the glycoside, the responses to NA and K are potentiated. Vascular responses to changes in extracellular K concentration are influenced by digoxin.