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+.

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.

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.

Some effects of the ionophore X-537A on the isolated rat tail artery

1978 ◽  
Vol 56 (3) ◽  
pp. 474-482 ◽  
Author(s):  
Vladimír Palatý ◽  
Mary E. Todd
Keyword(s):  
Smooth Muscle ◽  
Contractile Response ◽  
Rat Tail Artery ◽  
Concentration Gradients ◽  
Irreversible Loss ◽  
Tail Artery ◽  
Endogenous Catecholamines ◽  
Rat Tail ◽  
Isolated Rat ◽  
Stimulation Of

The effects of micromolar concentrations of the ionophore X-537A (RO 2-2985) were studied using isolated preparations of the rat tail artery. The ionophore causes complete release of catecholamines from adrenergic nerves, which is the sole cause of the transient contractile response. The amines are released by a nonexocytotic process which seems to be related to the ability of X-537A to act as an efficient transmembrane carrier of Na+, K+, and H+ The ionophore also causes an almost complete and irreversible loss of the cocaine-sensitive component of metaraminol uptake by the tissue. X-537A dissipates the transmembrane concentration gradients of Na and K in the smooth muscle component of the preparation. This effect is unrelated to the release of endogenous catecholamines, and it can also be observed after the Na pump has been inhibited with ouabain. It is fully reversible, though not readily, and it can be induced repeatedly. In catecholamine-depleted strips, X-537A dissipates the transmembrane Na+ and K+ gradients without causing any change in tension. Stimulation of the rate of O2 consumption by X-537A in catecholamine-depleted tissue is reversible, and it is unaffected by ouabain and (or) removal of external Ca2+.

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.

scholarly journals Palytoxin-induced contraction and release of endogenous noradrenaline in rat tail artery

1988 ◽  
Vol 95 (1) ◽  
pp. 183-188 ◽  
Author(s):  
H. Karaki ◽  
H. Nagase ◽  
Y. Ohizumi ◽  
N. Satake ◽  
S. Shibata
Keyword(s):  
Rat Tail Artery ◽  
Tail Artery ◽  
Endogenous Noradrenaline ◽  
Rat Tail

Desensitization of the vascular contractile response to cumulative doses of α2-adrenoceptor agonists

1986 ◽  
Vol 64 (10) ◽  
pp. 1343-1345 ◽  
Author(s):  
D. W. Cheung
Keyword(s):  
Dose Response ◽  
Saphenous Vein ◽  
Contractile Response ◽  
Rat Tail Artery ◽  
Contractile Responses ◽  
Tail Artery ◽  
Α2 Adrenoceptor ◽  
Adrenoceptor Agonists ◽  
Rat Tail

Contractile responses to single or cumulative doses of α-adrenoceptor agonists were compared in the tail artery and the saphenous vein of the rat. In the rat tail artery, there were no differences in the dose–response relationships to noradrenaline, methoxamine, and KCl whether the agonists were applied as single or cumulative doses. However, the responses to single doses of clonidine and B-HT 920 were significantly larger than similar doses applied cumulatively. In the rat saphenous vein, responses to single doses of noradrenaline, clonidine, and B-HT 920 were also significantly larger than the corresponding cumulative doses. However, there was no difference in the responses to KCl. It was suggested that desensitization of α2-adrenoceptors in these vessels may result in the diminished responses to cumulative doses of the agonists. Desensitization appeared to be specific to α2-adrenoceptors, since the effect was not observed in responses mediated by the α1-adrenoceptors and KCl.

Sign in / Sign up

Export Citation Format

Share Document