TY - JOUR
T1 - Relaxation of canine saphenous vein following brief transmural nerve stimulation
AU - Rooke, T. W.
AU - Rimele, T. J.
AU - Vanhoutte, P. M.
PY - 1983
Y1 - 1983
N2 - 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.
AB - 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.
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U2 - 10.1152/ajpheart.1983.245.6.h1073
DO - 10.1152/ajpheart.1983.245.6.h1073
M3 - Article
C2 - 6318571
AN - SCOPUS:0020997665
SN - 0363-6135
VL - 14
SP - H1073-H1076
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 6
ER -