Effects of U46619 on contractions to 5‐HT, sumatriptan and methysergide in canine coronary artery and saphenous vein <i>in vitro</i>

Kemp, B.; Cocks, T. M.

doi:10.1111/j.1476-5381.1995.tb15052.x

Cited by 13 publications

(10 citation statements)

References 27 publications

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“…the rabbit iliac artery (36). Similarly, U-46619 (7) and endogenous thromboxane (22) amplified sumatriptaninduced contraction in human coronary arteries, although U-46619 failed to potentiate sumatriptan-induced contraction in the dog coronary artery (21). Likewise, in the bovine pulmonary artery (25) and in the rabbit mesenteric artery (5), U-46619 also amplified sumatriptan-induced contraction.…”

Section: Discussionmentioning

confidence: 99%

“…Whereas this amplifying effect is well established in peripheral blood vessels (7,9,21,22), amplification of serotoninergic responses in cerebral vessels is considerably more controversial. Some limited studies have examined the ability of contractile agonists to amplify serotonininduced contraction in cerebral arteries from several species with conflicting results (2,12,18,19).…”

mentioning

confidence: 99%

“…For example, sumatriptan-induced peripheral vascular contraction has been widely studied in the rabbit saphenous vein (9), femoral artery (4), mesenteric artery (5), and iliac artery (36). Because the cardiovascular liabilities of sumatriptan may be related to its ability to constrict coronary arteries (23), sumatriptan has also been studied in coronary arteries from dogs (21) and humans (1). In contrast, the cerebral vascular effects of sumatriptan have been less extensively studied (3,16,17).…”

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confidence: 99%

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Amplification of sumatriptan-induced contraction in rabbit saphenous vein but not in basilar artery

Bhattacharya

Schenck

Cohen

2003

American Journal of Physiology-Heart and Circulatory Physiology

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. Amplification of sumatriptan-induced contraction in rabbit saphenous vein but not in basilar artery. Am J Physiol Heart Circ Physiol 284: H719-H726, 2003; 10.1152/ajpheart.00345.2002.-The modulation of serotonin (5-HT1B/1D) receptor-induced vascular contractility by histamine and U-46619 was compared in the rabbit basilar artery and saphenous vein. In the saphenous vein, histamine (5 ϫ 10 Ϫ7 M) significantly increased the potency (from pEC50 of 6.0 to 6.8) and efficacy (from 52.3% to 88.2%) of sumatriptan. Likewise, U-46619 (5 ϫ 10 Ϫ9 M) also increased the potency (from pEC50 of 5.9 to 6.6) and efficacy (from 51.8% to 92.1%) of sumatriptan in the saphenous vein. In contrast, equieffective concentrations of histamine (10 Ϫ7 M) and U-46619 (3 ϫ 10 Ϫ9 M) failed to amplify contraction to sumatriptan in the basilar artery. Contraction to sumatriptan was inhibited by nitrendipine (10 Ϫ7 M) in the basilar artery but not in the saphenous vein, suggesting that different contractile signaling mechanisms are operating in these tissues. Furthermore, U-46619-and thrombin-induced contractility in the basilar artery were also not amplified by histamine, suggesting that lack of amplification of contraction in the basilar artery was not restricted to sumatriptan but was rather a characteristic of this cerebral vessel. These data suggest that in the in vivo plasma milieu sumatriptan will more markedly contract the peripheral saphenous vein than the basilar artery, a cerebral blood vessel. nitrendipine; histamine; U-46619; serotonin receptors SUMATRIPTAN is an antimigraine drug (20) with a high affinity for serotonin 5-HT 1B and 5-HT 1D receptors (27). The antimigraine efficacy of sumatriptan has been attributed, in part, to its ability to activate central vascular 5-HT 1B/1D receptors (8). However, much of the information on the vascular effects of sumatriptan has been derived from studies using peripheral vascular serotonin receptors. For example, sumatriptan-induced peripheral vascular contraction has been widely studied in the rabbit saphenous vein (9), femoral artery (4), mesenteric artery (5), and iliac artery (36). Because the cardiovascular liabilities of sumatriptan may be related to its ability to constrict coronary arteries (23), sumatriptan has also been studied in coronary arteries from dogs (21) and humans (1). In contrast, the cerebral vascular effects of sumatriptan have been less extensively studied (3,16,17).Modest increases in vascular tone with threshold concentrations of vascular contractile agonists such as prostaglandin, angiotensin, histamine, endothelin, or adrenergic agonists are known to increase sumatriptaninduced vascular contractility (35). Whereas this amplifying effect is well established in peripheral blood vessels (7,9,21,22

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Amplification of sumatriptan-induced contraction in rabbit saphenous vein but not in basilar artery

Bhattacharya

Schenck

Cohen

2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…Contractile synergism between 5-hydroxytryptamine and other vasoconstrictor substances has been observed in a number of peripheral and cerebrovascular blood vessels (19). In some animal coronary artery models (20,21), as well as in human coronary arteries (22,23), a contractile synergistic effect between 5-hydroxytryptamine and U46619 has been demonstrated.…”

Section: Discussionmentioning

confidence: 94%

Effect of Somatostatin on Rabbit Isolated Coronary Arteries

Ruiz

Padilla

Tejerina

2002

Japanese Journal of Pharmacology

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ABSTRACT-Somatostatin analogues are capable of inhibiting vascular smooth muscle and endothelial cell proliferation. However, little is known about the effect of somatostatin on vascular responses in endothelium-denuded coronary arteries in vitro. The aim of this work was to determine whether or not somatostatin prevented the contractile response induced by 5-hydroxytryptamine and acetylcholine in endothelium-denuded rabbit coronary arteries. Somatostatin attenuated the contraction produced by 5-hydroxytryptamine in both proximal (PC) and distal coronary (DC) arteries (contraction induced by 10 -4 M 5-hydroxytryptamine was inhibited by 10 -6 M somatostatin by 90.8 ± 11.0% (P<0.001, n = 9) and by 46.2 ± 14.0% (P<0.05, n = 9) in DC and PC, respectively), but concentration-dependently decreased the contraction induced by U46619 (11a-epoxy-methanoprostaglandin F2=) only in PC arteries, suggesting that the response of PC and DC arteries to somatostatin were qualitatively different. Furthermore, we suggest that somatostatin may enhance acetylcholine-induced relaxation by combination of increasing endothelium-dependent relaxation (by a NO-dependent mechanism) and blocking contraction at the muscle level.Keywords: Somatostatin, Coronary artery, Acetylcholine, 5-Hydroxytryptamine, Nitric oxide Vascular diseases as well as surgical interventions such as coronary angioplasty induce endothelial denudation (1, 2) in coronary arteries. Loss of the endothelial layer alters vascular responses to certain agonists; thus 5-hydroxytryptamine and acetylcholine, which induce vasodilatation in normal coronary arteries, might be impaired or even turn into vasoconstriction in endothelium-denuded coronary arteries, leading to coronary spasm (1, 3, 4). In addition, thromboxane A2 released by platelets (5) is another candidate for the mediation of coronary vasospasm (6) since it is found in increasing concentration at the site of coronary arterial stenosis (7).Somatostatin (SRIF) is a neouroendocrine peptide (8) that exerts a wide range of physiological actions. However, the vascular effects of somatostatin are still unclear. A variety of studies have demonstrated species and regional differences in the blood flow responses to somatostatin. Thus, while in the rat superior mesenteric artery, octreotride (a somatostatin analogue) boosts vasoconstriction induced by a -agonists (9), in the vascular bed of cats, somatostatin showed opposite effects (10). On the other hand, we and others have shown that, although somatostatin has no effect on arteries kept under resting tension, it relaxes arteries precontracted with noradrenaline in vitro (11,12). Despite positive effects of somatostatin found in animal models of coronary restenosis, based on the antiproliferative effect of this peptide on both vascular smooth muscle (13) and endothelial cells (14, 15), little is known about the effect of somatostatin on vascular responses in endothelium-denuded coronary arteries. The purpose of this work was to determine whether or not somatostatin, in an 'in ...

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“…Functional study of vessel contraction with prepared aortic ring was carried out by cumulative treatment with U46619, a thromboxane A2 agonist (22), or phenylephrine, a α1-adrenergic agonist, to induce vessel contraction. Glucosamine treatment synergistically increased U46619-induced vessel contraction at sub-maximal concentration ( Fig.…”

Section: Glucosamine Treatment Increases Vessel Contraction Via the Rmentioning

confidence: 99%

Glucosamine increases vascular contraction through activation of RhoA/Rho kinase pathway in isolated rat aorta

Kim¹,

Seok²,

Kim³

et al. 2011

BMB Reports

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Diabetes is a well-known independent risk factor for vascular disease. However, its underlying mechanism remains unclear. It has been reported that increased influx of the hexosamine biosynthesis pathway (HBP) induces O-GlcNAcylation of proteins, leading to insulin resistance. In this study, we determined whether or not O-GlcNAc modification of proteins could increase vessel contraction. Using an endothelium-denuded aortic ring, we observed that glucosamine induced OGlcNAcylation of proteins and augmented vessel contraction stimulated by U46619, a thromboxane A2 agonist, via augmentation of the phosphorylation of MLC20, MYPT1(Thr855), and CPI17, but not phenylephrine. Pretreatment with OGT inhibitor significantly ameliorated glucosamine-induced vessel constriction. Glucosamine treatment also increased RhoA activity, which was also attenuated by OGT inhibitor. In conclusion, glucosamine, a product of glucose influx via the HBP in a diabetic state, increases vascular contraction, at least in part, through activation of the RhoA/Rho kinase pathway, which may be due to O-GlcNAcylation. [BMB reports 2011; 44(6): 415-420]

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Effects of U46619 on contractions to 5‐HT, sumatriptan and methysergide in canine coronary artery and saphenous vein in vitro

Cited by 13 publications

References 27 publications

Amplification of sumatriptan-induced contraction in rabbit saphenous vein but not in basilar artery

Amplification of sumatriptan-induced contraction in rabbit saphenous vein but not in basilar artery

Effect of Somatostatin on Rabbit Isolated Coronary Arteries

Glucosamine increases vascular contraction through activation of RhoA/Rho kinase pathway in isolated rat aorta

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