Release of noradrenaline from the rat tail artery induced by inhibition of the sodium pump in calcium-free solution

1981 ◽  
Vol 59 (4) ◽  
pp. 347-350 ◽  
Author(s):  
Vladimír Palatý
Keyword(s):  
Noradrenaline Release ◽  
Sodium Pump ◽  
Rat Tail Artery ◽  
Release Of Noradrenaline ◽  
Tail Artery ◽  
Storage Vesicles ◽  
Endogenous Noradrenaline ◽  
Electron Dense Core ◽  
Rat Tail ◽  
Isolated Rat

The release of noradrenaline from the isolated rat tail artery into Ca2+- and K-free, 1 mM ouabain containing solution was measured by means of radioenzymatic method. The rate of noradrenaline release increased gradually reaching a maximum of ca. 2.30 nmol∙g−1∙h−1 after 100 min. The enhancement of noradrenaline release could be inhibited by cocaine and phenoxybenzamine but not by desipramine. The rate of noradrenaline release could be approximately doubled by prior inhibition of monoamine oxidase with pargyline. The release was accompanied by a decline in the proportion of storage vesicles containing an electron-dense core. These observations indicate that, in the absence of external Ca2+, inhibition of the sodium pump causes nonexocytotic release of endogenous noradrenaline.

Release of endogenous noradrenaline from the rat tail artery induced by veratridine

1982 ◽  
Vol 60 (6) ◽  
pp. 805-810 ◽  
Author(s):  
Vladimír Palatý
Keyword(s):  
Sodium Pump ◽  
Rat Tail Artery ◽  
Free Solution ◽  
Release Of Noradrenaline ◽  
Tail Artery ◽  
Low Concentrations ◽  
Endogenous Noradrenaline ◽  
Increased Activity ◽  
Rat Tail ◽  
Isolated Rat

The overflow of endogenous noradrenaline from the isolated rat tail artery was measured using a radioenzymatic method. Veratridine increased the overflow markedly even in the absence of external Ca2+. Modifications of the effect of 5 μM veratridine by tetrodotoxin, pargyline, cocaine, lidocaine, and phenoxybenzamine indicated that interaction of the alkaloid with the sodium channel induces primarily nonexocytotic release of noradrenaline. Ouabain inhibited the effect of 5 μM veratridine on the overflow into Ca2+ -free solution, but it greatly potentiated the effect if external Ca2+ was present. Potentiation of the effect of veratridine in Ca2+-free solution by cyanide was ouabain sensitive. These observations are consistent with the hypothesis that, at low concentrations of veratridine such as 5 μM, the initial cause of enhanced release of noradrenaline may be a consequence of increased activity of the sodium pump, namely increased consumption of ATP by the pump.

Release of 3,4-dihydroxyphenylglycol from the rat tail artery induced by veratridine

1984 ◽  
Vol 62 (1) ◽  
pp. 151-152 ◽  
Author(s):  
Vladimír Palatý
Keyword(s):  
Amperometric Detection ◽  
Neuronal Uptake ◽  
Rat Tail Artery ◽  
Free Solution ◽  
Release Of Noradrenaline ◽  
Tail Artery ◽  
Storage Vesicles ◽  
Rat Tail ◽  
Isolated Rat ◽  
External K

The overflow of endogenous 3,4-dihydroxyphenylethylene glycol and noradrenaline from the isolated rat tail artery was measured by high pressure liquid chromatography with amperometric detection. Veratridine, but not elevated external K, caused a significant increase in the overflow of the glycol under conditions when formation of the latter from released noradrenaline was prevented by blockade of neuronal uptake1 with desipramine. The results support the hypothesis that, in addition to evoking exocytotic release of noradrenaline into Ca-containing solution, the alkaloid also increases leakage of noradrenaline from storage vesicles. The latter process seems responsible for veratridine-induced release of noradrenaline into Ca2+-free solution.

Inhibition of monoamine oxidase by amiloride

1985 ◽  
Vol 63 (12) ◽  
pp. 1586-1589 ◽  
Author(s):  
Vladimír Palatý
Keyword(s):  
Monoamine Oxidase ◽  
Brain Homogenate ◽  
Competitive Inhibitor ◽  
Rat Tail Artery ◽  
Monoamine Oxidase Activity ◽  
Tail Artery ◽  
Endogenous Noradrenaline ◽  
Rat Tail ◽  
Isolated Rat ◽  
External K

Amiloride was found to lower the overflow of 3,4-dihydroxyphenylethylene glycol from isolated rat tail artery. The overflow was reduced to about 50% in the presence of 10−5 M concentration of the drug. Reduced overflows of the glycol were observed also under conditions when the nonexocytotic release of endogenous noradrenaline was enhanced by tyramine, reserpine, or by the elevation of external K+ in the absence of extracellular Ca2+. They were accompanied by increased overflows of the amine. Amiloride inhibited monoamine oxidase activity (E.C. 1.4.3.4) of the A form in rat brain homogenate by acting as a competitive inhibitor.

Adenosine receptors involved in modulation of noradrenaline release in isolated rat tail artery

2004 ◽  
Vol 504 (1-2) ◽  
pp. 17-25 ◽  
Author(s):  
Carmen Diniz ◽  
Paula Fresco ◽  
Sandra Leal ◽  
Jorge Gonçalves
Keyword(s):  
Noradrenaline Release ◽  
Adenosine Receptors ◽  
Rat Tail Artery ◽  
Tail Artery ◽  
Rat Tail ◽  
Isolated Rat

The transient contractile response of the isolated rat tail artery to inhibition of the sodium pump

1980 ◽  
Vol 58 (4) ◽  
pp. 336-339 ◽  
Author(s):  
Vladimír Palatý
Keyword(s):  
Smooth Muscle ◽  
Sodium Pump ◽  
Contractile Response ◽  
Physiological Salt Solution ◽  
Rat Tail Artery ◽  
Active Tension ◽  
Tail Artery ◽  
Endogenous Catecholamines ◽  
Rat Tail ◽  
Isolated Rat

The isolated rat tail artery responds to incubation in 1 mM ouabain containing, K-free physiological salt solution by transient contraction which is due to release of endogenous catecholamines. The eventual decline in active tension cannot be attributed solely to the decreasing rate of release of endogenous catecholamines, for the latter remains quite high even after the preparation has relaxed completely. It seems, therefore, that the relaxation is due also to the substantial decrease in the responsiveness of smooth muscle cells to (−)-norepinephrine that accompanies dissipation of the transmembrane gradients of Na+ and K+.

Sign in / Sign up

Export Citation Format

Share Document