The ability of electrical stimulation to cause relaxation in the canine saphenous vein was evaluated. Rings of vein were studied isometrically in organ chambers containing physiological salt solution. Prostaglandin F(2α) produced stable contractions during which brief periods of electrical stimulation caused further contraction. With cessation of the electrical stimulation, tension transiently decreased to a level below that observed prior to the stimulation (undershoot). This poststimulation undershoot was blocked by tetrodotoxin, phentolamine, ouabain, and potassium-free solution; it was not affected by atropine, cimetidine, indomethacin, ketanserin, methysergide, propranolol, pyrilamine, or removal of the endothelium. Undershoot did not occur following electrical stimulation during contractions evoked by norepinephrine. During superfusion with PGF(2α), a brief exposure to exogenous norepinephrine caused a transient contraction followed by a subsequent undershoot. These results suggest that 1) the interaction of norepinephrine with postjunctional α-adrenoceptors on vascular smooth muscle leads to an increase in the activity of Na+K+-ATPase, and 2) increased activity of Na+-K+-ATPase is responsible for the poststimulation undershoot.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Jan 1 1983|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)