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