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.

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 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 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.

Effects of Urotensin I on the Isolated Rat Tail Artery

Pharmacology ◽  
1979 ◽  
Vol 18 (2) ◽  
pp. 72-79 ◽  
Author(s):  
M.E. Gerritsen ◽  
K. Lederis
Keyword(s):  
Rat Tail Artery ◽  
Tail Artery ◽  
Rat Tail ◽  
Isolated Rat

Three different vasoactive responses of rat tail artery to nicotine

1999 ◽  
Vol 78 (1) ◽  
pp. 20-28
Author(s):  
Rui Wang ◽  
Zunzhe Wang
Keyword(s):  
Smooth Muscles ◽  
Rat Tail Artery ◽  
Vascular Smooth Muscles ◽  
Vascular Effects ◽  
Tail Artery ◽  
Complete Relaxation ◽  
Underlying Mechanisms ◽  
Channel Currents ◽  
Rat Tail ◽  
Isolated Rat

The vasoactive effects of nicotine on isolated rat tail artery tissues were studied. Nicotine transiently contracted rat tail artery tissues (EC50, 55.6 ± 2 µM) in an extracellular Ca2+ dependent and endothelium-independent fashion. The blockade of alpha1-adrenoceptors, but not alpha2-adrenoceptors or P2X purinoceptors, inhibited the nicotine-induced contraction by 38 ± 7% (p < 0.05). Nicotine (1 mM) depolarized membrane by 13 ± 3 mV, but did not affect L-type Ca2+ channel currents, of the isolated rat tail artery smooth muscle cells. The phenylephrine-precontracted tail artery tissues were relaxed by nicotine (EC50, 0.90 ± 0.31 mM), which was significantly inhibited after the blockade of nicotinic receptors. Simultaneous removal of phenylephrine and nicotine, after a complete relaxation of the phenylephrine-precontracted tail artery strips was achieved by nicotine at accumulated concentrations (>=10 mM), triggered a Ca2+-dependent rebound long-lasting vasoconstriction (n = 20). This rebound contraction was abolished in the absence of calcium or in the presence of tetracaine in the bath solution. Pretreatment of vascular tissues with a nicotinic receptor antagonist did not affect the nicotine-induced vasoconstriction or nicotine withdrawal induced rebound contraction. The elucidation of the triphasic vascular effects of nicotine and the underlying mechanisms is important for a better understanding of the complex vascular actions of nicotine.Key words: nicotine, smokeless tobacco, vascular smooth muscles, contraction, relaxation.

Amiloride acts as an α-adrenergic antagonist in the isolated rat tail artery

1986 ◽  
Vol 64 (7) ◽  
pp. 931-933 ◽  
Author(s):  
Vladimír Palatý
Keyword(s):  
Contractile Response ◽  
Krebs Solution ◽  
Rat Tail Artery ◽  
Tail Artery ◽  
Adrenergic Antagonist ◽  
Adrenergic Transmission ◽  
Endogenous Noradrenaline ◽  
Site Of Action ◽  
Postsynaptic Site ◽  
Rat Tail

In the final concentration of 100 μM, amiloride increased substantially the overflow of endogenous noradrenaline and decreased that of 3,4-dihydroxyphenylethylene glycol from the rat tail artery into Krebs solution supplemented with 10 μM veratridine. The overflow of the amine into a 120 mM-K version of Krebs solution was unaffected by amiloride, while that of the glycol was reduced. Abolition of the contractile response to 10 μM veratridine by 2 μM phentolamine indicated that the response was due to release of endogenous noradrenaline. Addition of amiloride in the final concentrations of 10 and 100 μM caused relaxation of strips contracted by the alkaloid. The dose–response relations for exogenous noradrenaline measured in the absence or presence of 50 μM amiloride indicated that the drug acted as a reversible competitive α-adrenergic antagonist. The phentolamine-resistant component of the contractile response to the 120 mM-K solution was unaffected by 100 μM amiloride. Although the exact site of action of amiloride remains to be determined, it can be concluded that amiloride inhibits adrenergic transmission at a postsynaptic site at a step preceding elevation of myoplasmic Ca2+.

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