Constriction of the Smooth Muscle of Rat Tail and Femoral Arteries and Dog Saphenous Vein Is Induced by Uridine Triphosphate via ‘Pyrimidinoceptors’, and by Adenosine Triphosphate via P2x Purinoceptors

1990 ◽  
Vol 27 (6) ◽  
pp. 352-364 ◽  
Author(s):  
Bernard Saïag ◽  
Dominique Milon ◽  
Hervé Allaín ◽  
Bernard Rault ◽  
Jean Van Den Driessche
1978 ◽  
Vol 235 (5) ◽  
pp. H581-H586
Author(s):  
O. Beaty ◽  
R. R. Lorenz ◽  
J. T. Shepherd

In dog saphenous vein strips, decreases in extracellular sodium from 5% to 23% did not alter basal tension, but progressively increased tension developed during electrical stimulation (1.0 to 10 Hz). The augmentation did not occur with similar reductions in chloride ions. When osmolality was maintained with sucrose, the response to electrical stimulation also was enhanced with a 5% reduction in sodium ions, but did not increase further with larger sodium reductions. The enhancement was due to some effect on the smooth muscle cells, because the overflow of [7-3H]norepinephrine during electrical stimulation was unaffected by the sodium reduction, whereas contractions caused by norepinephrine and barium chloride were potentiated. The potentiation did not depend on increased influx of extracellular calcium, because contractions induced by acetylcholine were unaffected by sodium reduction; and after blocking calcium influx with verapamil, the norepinephrine contractions still were augmented. It was concluded that a decrease in extracellular sodium by 5% (from the normal value of 143.3--131.1 meq/1) can enhance the response of venous smooth muscle to adrenergic stimuli.


1992 ◽  
Vol 105 (3) ◽  
pp. 603-608 ◽  
Author(s):  
Michael J. Sumner ◽  
Wasyl Feniuk ◽  
Julie D. McCormick ◽  
Patrick P. A. Humphrey

1991 ◽  
Vol 69 (8) ◽  
pp. 1184-1189 ◽  
Author(s):  
Z. L. Wang ◽  
C. Y. Kwan ◽  
A. Ohta ◽  
M. C. Chen

The effects of two structurally similar pyrazine derivatives, tetramethylpyrazine (TMP) and tetraethylpyrazine (TEP) on the contractile responses of dog saphenous vein to KCl (via membrane depolarization), phenylephrine (PHE, α1-adrenergic agonist), and B-HT 920 (α2-adrenergic agonist) were investigated. The relaxant or inhibitory effect of TMP and TEP was most potent on KCl-induced responses and least potent on PHE-induced responses. Their effect on KCl-induced responses was more prominent at 30 mM KCl than at 100 mM KCl. In Ca2+-free medium, PHE and B-HT 920 elicited transient responses, which were also markedly and reversibly inhibited by TMP and TEP. Similar results were also obtained when prostaglandin F2α was used as an agonist. In all four types of contractile responses involving different receptors, the inhibitory effect of TEP was consistently more potent than that of TMP. We conclude that both TMP and TEP behave as a nonselective smooth muscle relaxant having similar and multiple actions including their general interference with the processes involving both Ca2+ entry and intracellular Ca2+ release.Key words: vascular smooth muscle, calcium channels, tetramethylpyrazine, tetraethylpyrazine, α-adrenoceptors, saphenous vein.


1990 ◽  
Vol 64 (01) ◽  
pp. 091-096 ◽  
Author(s):  
W J Janssens ◽  
F J S Cools ◽  
L A M Hoskens ◽  
J M Van Nueten

SummaryRidogrel (6.3 × 10−6 to 10−4 M) inhibited contractions of isolated rat caudal arteries and rabbit femoral arteries caused by U-46619. The slope of an Arunlakshana-Schild plot (pA2-value: 3.4 × 10−6 M) on the caudal artery was slightly higher than one (1.14). This effect was maximal within}D min of incubation of the blood vessel with the compound and easily reversible. Ridogrel antagonised contractions of isolated rabbit femoral arteries caused by prostaglandin Fzo2α in the same concentration range. Ridogrel also inhibited contractions induced by aggregating rat platelets on isolated rat caudal arteries (itt the presence of ketanserin 4 × 10−7 M) and on isolated rabbit pulmonary and femoral arteries (in the absence of ketanserin). Ridogrel had no effect on Ca2+-induced contractions in depolarised isolated rabbit femoral arteries, and at 10−4 M antagonised serotonin-induced contractions in this blood vessel. Its effect on serotonin-induced contractions was statistically significant but very small on isolated rat caudal arteries. These observations indicate that ridogrel is an antagonist of prostaglandin endoperoxide/thromboxane A2 and prostaglandin F2α raCeptors on vascular smooth muscle.


2011 ◽  
Vol 15 (8) ◽  
pp. 1695-1702 ◽  
Author(s):  
Guanghong Jia ◽  
Anshu Aggarwal ◽  
Amanuel Yohannes ◽  
Deepak M. Gangahar ◽  
Devendra K. Agrawal

Sign in / Sign up

Export Citation Format

Share Document