Prejunctional α2A-autoreceptors in the canine saphenous vein

1997 ◽  
Vol 356 (3) ◽  
pp. 368-373 ◽  
Author(s):  
M. Q. Paiva ◽  
A. Mota ◽  
D. Moura ◽  
S. Guimarães
1987 ◽  
Vol 65 (3) ◽  
pp. 427-432 ◽  
Author(s):  
M. P. J. Senaratne ◽  
R. L. Jayakody ◽  
C. T. Kappagoda

This study was undertaken to assess the effects of exogenous α-agonists on the effector response to transmural nerve stimulation in canine saphenous vein rings. The response to a fixed train (5 s duration) of transmural nerve stimulation (8 Hz, 0.3 ms, 9 V) applied every 5 min was determined in the control state and in the presence of subthreshold (for contraction) concentrations of noradrenaline, adrenaline, clonidine, and methoxamine. The maximum potentiations achieved by the three drugs were 246.2 ± 36.9, 220.5 ± 38.8, 384.3 ± 78.7, and 353.3 ± 68.0%, respectively. The potentiation observed was significantly inhibited by indomethacin (10−6 mol/L) and propranolol (5 × 10−6 mol/L). Both indomethacin and propranolol potentiated the response to transmural nerve stimulation. The potentiation of the responses to transmural nerve stimulation by α-agonists suggests that, presynaptic α2-inhibition by circulating catecholamines is likely to be of limited biological significance in modulating the effector responses in the canine saphenous vein.


1983 ◽  
Vol 245 (6) ◽  
pp. H1073-H1076 ◽  
Author(s):  
T. W. Rooke ◽  
T. J. Rimele ◽  
P. M. Vanhoutte

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 F2 alpha 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 PGF2 alpha, 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 alpha-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.


Hypertension ◽  
1991 ◽  
Vol 18 (4) ◽  
pp. 516-522 ◽  
Author(s):  
L W Cress ◽  
W Freas ◽  
F Haddy ◽  
S M Muldoon

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