Extraneuronal effects of 6-hydroxydopamine and extraneuronal uptake of noradrenaline

1976 ◽  
Vol 173 (1) ◽  
Author(s):  
K. Unsicker ◽  
I.J. Allan ◽  
D.F. Newgreen
1979 ◽  
Vol 57 (12) ◽  
pp. 1443-1447 ◽  
Author(s):  
Edwin K. Jackson ◽  
William B. Campbell

In the isolated perfused rat mesentery, angiotensin II (3 × 10−9 M) in subpressor doses enhanced the vasoconstrictor responses to noradrenaline by 9.6 ± 1.4 mmHg. However, in mesenteries obtained from rats chemically sympathectomized with 6-hydroxydopamine, angiotensin II was without effect. Treatment of mesenteries with the noradrenaline neuronal uptake blockers desmethylimipramine (10−10 M), protriptyline (10−10 M), or cocaine (10−6 M) potentiated responses to noradrenaline by 3.8 ± 0.84, 3.7 ± 0.67, and 5.5 ± 0.26 mmHg, respectively. Angiotensin II alone or in combination with either desmethylimipramine, protriptyline, or cocaine potentiated the noradrenaline responses to a similar extent. On the other hand, corticosterone (1.5 × 10−6 M), an extraneuronal uptake blocker, enhanced noradrenaline responses by 4.3 ± 1.4 mmHg, and this enhancement was additive with the potentiation produced by cocaine and (or) angiotensin II. We conclude that angiotensin II in subpressor doses acts presynaptically to block selectively the neuronal uptake of noradrenaline without any appreciable effect on extraneuronal uptake.


1985 ◽  
Vol 72 (2) ◽  
pp. 94-95
Author(s):  
Pham Huu Chanh ◽  
R. Kaiser ◽  
R. Chahine ◽  
K. Abou Khalil ◽  
M. Abou-Assaly ◽  
...  

1992 ◽  
Vol 346 (2) ◽  
pp. 166-172 ◽  
Author(s):  
V. Marino ◽  
I. S. de la Laude ◽  
D. A. S. Parker ◽  
J. Dally ◽  
S. Wing

1976 ◽  
Vol 54 (2) ◽  
pp. 93-100 ◽  
Author(s):  
D. S. Golko ◽  
D. M. Paton

The characteristics of uptake of (±)-[β-14C]ephedrine were studied in isolated rabbit atria. Ephedrine was rapidly accumulated against the concentration gradient. From 5 × 10−7 to 10−2 M, uptake occurred at a uniform initial rate. Uptake was slightly inhibited by high concentrations of ouabain, cocaine, desipramine, lidocaine and phenethylamines, and by a reduction in the external Na+ concentration. Uptake was not, however, reduced by omission of K+ from the medium, by metabolic inhibitors or by a variety of drugs known to inhibit the extraneuronal uptake and binding of noradrenaline. Pretreatment of animals with 6-hydroxydopamine very significantly reduced the uptake of (±)-[3H]metaraminol, but did not alter the uptake of ephedrine. It was concluded that the uptake of ephedrine in rabbit atria occurred predominantly in extraneuronal tissues possibly as a result of passive diffusion followed by binding.


1985 ◽  
Vol 63 (4) ◽  
pp. 298-303 ◽  
Author(s):  
Paul M. Lundy ◽  
Sharunas Gverzdys ◽  
Robert Frew

Ketamine (1.1 × 10−5 to 3.7 × 10−4 M) potentiated catecholamine responses of rat anococcygeus muscle and rabbit aorta in vitro. In the anococcygeus, potentiation was abolished by cocaine (2.9 × 10−5 M) pretreatment or by chemical sympathectomy using 6-hydroxydopamine (6-OHDA), but was unaffected by pretreatment with the extraneuronal uptake inhibitor cortisol (8.3 × 10−5 M), or the catechol-O-methyltransferase inhibitor tropolone (2.4 × 10−4 M). The action of ketamine mimicked the potentiating effect of cocaine on tyramine responses. In contrast, the potentiation by ketamine in rabbit aorta was unaffected by cocaine or 6-OHDA but was abolished by cortisol or tropolone; and ketamine potentiated tyramine responses, whereas cocaine inhibited them. Thus the mechanism of action by which ketamine produces potentiation of catecholamines in these two tissues is completely different. These results suggest that ketamine has the unusual ability to block neuronal and extraneuronal uptake and that the predominating mechanism will depend on the type of tissue examined and the morphology of its adrenergic innervation.


1995 ◽  
Vol 10 (3) ◽  
pp. 151-153 ◽  
Author(s):  
Jörg Babin-Ebell ◽  
Martin Gliese

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