α1A-Adrenoceptors, but not α1B- or α1D-adrenoceptors, contribute to enhanced contractile response to phenylephrine in cooling conditions in the rat tail artery

2018 ◽  
Vol 838 ◽  
pp. 120-128 ◽  
Author(s):  
Hirotake Ishida ◽  
Shin-ya Saito ◽  
Tomohisa Ishikawa
1986 ◽  
Vol 64 (7) ◽  
pp. 931-933 ◽  
Author(s):  
Vladimír Palatý

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+.


1978 ◽  
Vol 56 (3) ◽  
pp. 474-482 ◽  
Author(s):  
Vladimír Palatý ◽  
Mary E. Todd

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+.


1986 ◽  
Vol 64 (10) ◽  
pp. 1343-1345 ◽  
Author(s):  
D. W. Cheung

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.


1980 ◽  
Vol 58 (4) ◽  
pp. 336-339 ◽  
Author(s):  
Vladimír Palatý

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+.


2020 ◽  
Vol 182 ◽  
pp. 114263
Author(s):  
F. Fusi ◽  
P. Mugnai ◽  
A. Trezza ◽  
O. Spiga ◽  
G. Sgaragli

2007 ◽  
Vol 135 (1-2) ◽  
pp. 130
Author(s):  
James A. Brock ◽  
Diana Tripovic ◽  
Svetlana Pianova ◽  
Elspeth M. McLachlan

1991 ◽  
Vol 22 (2) ◽  
pp. 399-402 ◽  
Author(s):  
Xie-Nan Huang ◽  
Issei Takayanagi ◽  
Ryuichi Kurata ◽  
Tetsuhiro Hisayama

1980 ◽  
Vol 164 (3) ◽  
pp. 252-256 ◽  
Author(s):  
R. C. Webb ◽  
P. M. Vanhoutte ◽  
D. F. Bohr

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