Garan H, Powers E R, Ruskin J N, Powell W J
Am J Physiol. 1980 May;238(5):H729-39. doi: 10.1152/ajpheart.1980.238.5.H729.
This study was undertaken to investigate the effect of intravenous acetylstrophanthidine and digoxin on the gracilis vascular resistance of hypotensive dogs. The gracilis muscle was isolated and separately perfused, but the nerve to the muscle was left intact. Acetylstrophanthidin, 0.5 mg iv, and digoxin, 1.0 mg iv, both produced a sustained vasodilator response in the gracilis vascular bed of all the hypotensive animals (mean arterial pressure 50 mmHg). A short-lasting vasoconstriction preceded the vasodilation in response to acetylstrophanthidin in 6 of the 8 animals. Prior local alpha-adrenergic blockade with phenoxybenzamine did not have any significant effect on vasodilation. Prior local cholinergic receptor blockade with atropine, however, abolished the sustained vasodilator response, thus indicating that the mechanism responsible for this neurogenic effect is cholinergic. In contrast, in the normotensive dogs, the response to intravenously administered digoxin was sustained vasoconstriction, which was abolished by prior local alpha-adrenergic receptor blockade. Thus, the effect of digitalis glycosides on peripheral vascular resistance is importantly affected by the background level of sympathetic activity.