Long-lasting physiological antagonism of calcitonin gene-related peptide towards endothelin-1 in rat mesenteric arteries and human coronary arteries

Labruijere, Sieneke; Compeer, Matthijs G.; Bogaerdt, Antoon J. van den; MaassenVanDenBrink, Antoinette; Mey, Jo G. R. De; Danser, A.H. Jan; Batenburg, Wendy W.

doi:10.1016/j.ejphar.2013.10.012

Cited by 9 publications

(6 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This might be explained by differential anatomical origin of the investigated artery segments as this can be a determinant of adrenoceptor distribution (i.e., receptor subtype and density) or by differential sympathetic innervation (Guimaraes and Moura 2001). Interestingly, our estimated potencies of adrenergic agonists in mouse MRA are in agreement with results obtained in rat mesenteric arteries (Nielsen and Mulvany 1990;Buus et al 1994;Dhawan et al 2004;Labruijere et al 2013) and slightly lower than those reported from studies on human mesenteric arteries (Muller-Schweinitzer et al 1997;Hutri-Kahonen et al 1999;Ferrero et al 2013).…”

Section: Discussionsupporting

confidence: 92%

See 1 more Smart Citation

Translational value of mechanical and vasomotor properties of mouse isolated mesenteric resistance‐sized arteries

Outzen

Zaki

Abdolalizadeh

et al. 2015

Pharmacology Res & Perspec

View full text Add to dashboard Cite

Mice are increasingly used in vascular research for studying perturbations and responses to vasoactive agents in small artery preparations. Historically, small artery function has preferably been studied in rat isolated mesenteric resistance‐sized arteries (MRA) using the wire myograph technique. Although different mouse arteries have been studied using the wire myograph no establishment of optimal settings has yet been performed. Therefore, the purposes of this study were firstly to establish the optimal settings for wire myograph studies of mouse MRA and compare them to those of rat MRA. Second, by surveying the literature, we aimed to evaluate the overall translatability of observed pharmacological vasomotor responses of mouse MRA to those obtained in rat MRA as well as corresponding and different arteries in terms of vessel size and species origin. Our results showed that the optimal conditions for maximal active force development in mouse MRA were not significantly different to those determined in rat MRA. Furthermore, we found that the observed concentration‐dependent vasomotor responses of mouse MRA to noradrenaline, phenylephrine, angiotensin II, sarafotoxin 6c, 5‐hydroxytryptamine, carbachol, sodium nitroprusside, and retigabine were generally similar to those described in rat MRA as well as arteries of different sizes and species origin. In summary, the results of this study provide a framework for evidence‐based optimization of the isometric wire myograph setup to mouse MRA. Additionally, in terms of translational value, our study suggests that mouse MRA can be applied as a useful model for studying vascular reactivity.

show abstract

Section: Discussionsupporting

confidence: 92%

“…; Labruijere et al. ) and slightly lower than those reported from studies on human mesenteric arteries (Muller‐Schweinitzer et al. ; Hutri‐Kahonen et al.…”

Section: Discussionmentioning

confidence: 82%

Translational value of mechanical and vasomotor properties of mouse isolated mesenteric resistance‐sized arteries

Outzen

Zaki

Abdolalizadeh

et al. 2015

Pharmacology Res & Perspec

View full text Add to dashboard Cite

show abstract

“…), but is present in human coronary arteries (Labruijere et al . ) and in rats in vivo (Meens et al . ).…”

Section: Endothelium‐dependent Contractionsmentioning

confidence: 99%

Endothelial dysfunction and vascular disease - a 30th anniversary update

Vanhoutte¹,

et al. 2016

View full text Add to dashboard Cite

The endothelium can evoke relaxations of the underlying vascular smooth muscle, by releasing vasodilator substances. The best-characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO) which activates soluble guanylyl cyclase in the vascular smooth muscle cells, with the production of cyclic guanosine monophosphate (cGMP) initiating relaxation. The endothelial cells also evoke hyperpolarization of the cell membrane of vascular smooth muscle (endothelium-dependent hyperpolarizations, EDH-mediated responses). As regards the latter, hydrogen peroxide (H O ) now appears to play a dominant role. Endothelium-dependent relaxations involve both pertussis toxin-sensitive G (e.g. responses to α -adrenergic agonists, serotonin, and thrombin) and pertussis toxin-insensitive G (e.g. adenosine diphosphate and bradykinin) coupling proteins. New stimulators (e.g. insulin, adiponectin) of the release of EDRFs have emerged. In recent years, evidence has also accumulated, confirming that the release of NO by the endothelial cell can chronically be upregulated (e.g. by oestrogens, exercise and dietary factors) and downregulated (e.g. oxidative stress, smoking, pollution and oxidized low-density lipoproteins) and that it is reduced with ageing and in the course of vascular disease (e.g. diabetes and hypertension). Arteries covered with regenerated endothelium (e.g. following angioplasty) selectively lose the pertussis toxin-sensitive pathway for NO release which favours vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. In addition to the release of NO (and EDH, in particular those due to H O ), endothelial cells also can evoke contraction of the underlying vascular smooth muscle cells by releasing endothelium-derived contracting factors. Recent evidence confirms that most endothelium-dependent acute increases in contractile force are due to the formation of vasoconstrictor prostanoids (endoperoxides and prostacyclin) which activate TP receptors of the vascular smooth muscle cells and that prostacyclin plays a key role in such responses. Endothelium-dependent contractions are exacerbated when the production of nitric oxide is impaired (e.g. by oxidative stress, ageing, spontaneous hypertension and diabetes). They contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive and diabetic patients. In addition, recent data confirm that the release of endothelin-1 can contribute to endothelial dysfunction and that the peptide appears to be an important contributor to vascular dysfunction. Finally, it has become clear that nitric oxide itself, under certain conditions (e.g. hypoxia), can cause biased activation of soluble guanylyl cyclase leading to the production of cyclic inosine monophosphate (cIMP) rather than cGMP and hence causes contraction rather than relaxation of the underlying vascular smooth muscle.

show abstract

“…demonstrated that CGRP has protective effects on ischaemic neurons by reducing the apoptosis of neurons in rats following CI/R. A functional antagonism between ET‐1 and CGRP has been detected in rat mesenteric arteries and human coronary arteries [30]. During cerebral ischaemia, the dynamic balance between ET‐1 and CGRP can be disturbed, then the cerebral vascular will contract, aggravate cerebral ischaemia and hypoxia, and cause damage to brain cells.…”

Section: Discussionmentioning

confidence: 99%

Catalpol provides protective effects against cerebral ischaemia/reperfusion injury in gerbils

Liu

Suo³

et al. 2014

Journal of Pharmacy and Pharmacology

View full text Add to dashboard Cite

show abstract

Long-lasting physiological antagonism of calcitonin gene-related peptide towards endothelin-1 in rat mesenteric arteries and human coronary arteries

Cited by 9 publications

References 22 publications

Translational value of mechanical and vasomotor properties of mouse isolated mesenteric resistance‐sized arteries

Translational value of mechanical and vasomotor properties of mouse isolated mesenteric resistance‐sized arteries

Endothelial dysfunction and vascular disease - a 30th anniversary update

Catalpol provides protective effects against cerebral ischaemia/reperfusion injury in gerbils

Contact Info

Product

Resources

About