Two different biophases for adrenaline released by electrical stimulation or tyramine from the sympathetic nerve endings of the dog saphenous vein

1981 ◽  
Vol 316 (3) ◽  
pp. 200-204 ◽  
Author(s):  
S. Guimar�es ◽  
M. Q. Paiva
1980 ◽  
Vol 239 (2) ◽  
pp. H238-H246 ◽  
Author(s):  
D. K. Rorie ◽  
S. M. Muldoon ◽  
G. M. Tyce

The relative importance of neuronal and extraneuronal uptake in the disposition of norepinephrine (NE) released by electrical stimulation (ES) from adrenergic nerves in isolated dog saphenous vein was determined. Helical strips of vein were incubated in L-[7-(3)H]NE (1 x 10(-6)M) and mounted for superfusion. Superfusate was collected continuously before, during, and after ES (10 V; 2 ms; 1, 2, and 5 Hz). Measurements were made of [3H]NE and its metabolites in vein and in superfusate. Previous studies have established that 3,4-dihydroxyphenylglycol (DOPEG) is of neuronal origin and O-methylated metabolites (OMM) are of extraneuronal origin. Thus, extraneuronal uptake was estimated directly by measuring the amounts of OMM in superfusate, and neuronal uptake followed by metabolism was estimated by measuring [3H]DOPEG. The magnitude of the neuronal uptake fraction that enters vesicles for reuse was estimated from the compensatory increases in [3H]NE and in OMM when neuronal uptake was blocked. Similar amounts of released NE were taken up by neuronal uptake, by extraneuronal uptake, and diffused out of the synaptic cleft. Between 5-20% of the released NE was sequestered in vesicles for reuse.


1989 ◽  
Vol 257 (6) ◽  
pp. H1945-H1951 ◽  
Author(s):  
D. K. Rorie ◽  
L. W. Hunter ◽  
G. M. Tyce

Dihydroxyphenylglycol (DOPEG), the metabolite of norepinephrine (NE) that arises intraneuronally, was measured together with NE in superfusates collected before, during, and after nerve stimulation and in extracts of dog saphenous vein after superfusion and electrical stimulation (ES). Different concentrations of NE in the synaptic clefts were achieved by treating tissues with corticosterone, corticosterone and yohimbine, corticosterone and cocaine, or by omitting drugs from the superfusate. NE and DOPEG were quantitated by liquid chromatography with electrochemical detection. The time courses of NE overflow and DOPEG efflux into superfusate were followed. The amounts of DOPEG in superfusates under basal conditions were two to four times higher than the amounts of NE and progressively increased during ES except in tissues with neuronal uptake inhibited. NE overflow reached a steady state within the first 6 min of ES. Increased NE concentrations in synaptic clefts resulted in increased DOPEG production except where neuronal uptake was inhibited. The increased DOPEG production during ES appears to reflect the increased rate of neuronal uptake, which results in more NE being available for intraneuronal metabolism. No evidence was found that newly formed DOPEG was delayed in leaving the tissue. Thus the increase in DOPEG production that occurs during ES may be useful as an index of neuronal uptake of NE in dog saphenous vein.


1978 ◽  
Vol 235 (5) ◽  
pp. H581-H586
Author(s):  
O. Beaty ◽  
R. R. Lorenz ◽  
J. T. Shepherd

In dog saphenous vein strips, decreases in extracellular sodium from 5% to 23% did not alter basal tension, but progressively increased tension developed during electrical stimulation (1.0 to 10 Hz). The augmentation did not occur with similar reductions in chloride ions. When osmolality was maintained with sucrose, the response to electrical stimulation also was enhanced with a 5% reduction in sodium ions, but did not increase further with larger sodium reductions. The enhancement was due to some effect on the smooth muscle cells, because the overflow of [7-3H]norepinephrine during electrical stimulation was unaffected by the sodium reduction, whereas contractions caused by norepinephrine and barium chloride were potentiated. The potentiation did not depend on increased influx of extracellular calcium, because contractions induced by acetylcholine were unaffected by sodium reduction; and after blocking calcium influx with verapamil, the norepinephrine contractions still were augmented. It was concluded that a decrease in extracellular sodium by 5% (from the normal value of 143.3--131.1 meq/1) can enhance the response of venous smooth muscle to adrenergic stimuli.


2001 ◽  
Vol 38 ◽  
pp. S39-S42 ◽  
Author(s):  
Hirotoshi Kitagawa ◽  
Toji Yamazaki ◽  
Tsuyoshi Akiyama ◽  
Hidezo Mori ◽  
Kenji Sunagawa

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