British Journal of Pharmacology (BRIT J PHARMACOL)

Publisher: British Pharmacological Society, Wiley

Journal description

All aspects of experimental pharmacology including: Cellular and molecular pharmacology Biochemical pharmacology Neuroscience All aspects of general pharmacology Special Reports for rapid publication of important new results of special pharmacological significance The British Journal of Pharmacology is the leading 'original papers' publication in the field of general pharmacology.

Journal Impact: 1.64*

*This value is calculated using ResearchGate data and is based on average citation counts from work published in this journal. The data used in the calculation may not be exhaustive.

Journal impact history

2016 Journal impact Available summer 2017
2015 Journal impact 1.64
2014 Journal impact 1.55
2013 Journal impact 0.80
2012 Journal impact 1.29
2011 Journal impact 8.63
2010 Journal impact 7.37
2009 Journal impact 6.39
2008 Journal impact 4.84
2007 Journal impact 3.60
2006 Journal impact 4.12
2005 Journal impact 3.10
2004 Journal impact 2.17
2003 Journal impact 1.92
2002 Journal impact 1.98
2001 Journal impact 1.92
2000 Journal impact 1.82

Journal impact over time

Journal impact

Additional details

Cited half-life 7.50
Immediacy index 1.51
Eigenfactor 0.05
Article influence 1.32
Website British Journal of Pharmacology website
Other titles British journal of pharmacology, BJP, Proceedings of the British Pharmacological Society
ISSN 0007-1188
OCLC 1240522
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

This journal may support self-archiving.
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Publications in this journal

  • [Show abstract] [Hide abstract] ABSTRACT: The continued focus of attention on the diversity of mechanisms underpinning inflammation has improved our understanding of the potential to target specific pathways in the inflammatory network to achieve meaningful therapeutic gains. In this themed issue of the British Journal of Pharmacology our scope was deliberately broad, ranging across both acute and chronic disease in various organs. Pro- and anti-inflammatory mechanisms receive attention as does the phenotype of macrophages. Whilst the manifestations of neuro-inflammation are less obvious than those in peripheral tissues, central innate and adaptive immunity in brain and the M1/M2 phenotypes of microglia are topics of special interest. The contributions to the inflammatory milieu of cytokines, chemokines and associated signalling cascades are considered. Overall, the coverage herein advances the basic science underpinning our understanding of inflammation and emphasizes its importance in different pathologies. Linked ArticlesThis article is part of a themed section on Inflammation: maladies, models, mechanisms and molecules. To view the other articles in this section visit
    Article · Feb 2016 · British Journal of Pharmacology
  • [Show abstract] [Hide abstract] ABSTRACT: BACKGROUND AND PURPOSE The carbazole alkaloid murrayafoline A (MuA) enhances contractility and the Ca2+ currents carried by the Cav1.2 channels [ICa1.2] of rat cardiomyocytes. As only few drugs stimulate ICa1.2, this study was designed to analyse the effects ofMuA on vascular Cav1.2 channels. EXPERIMENTAL APPROACH Vascular activity was assessed on rat aorta rings mounted in organ baths. Cav1.2 Ba2+ current [IBa1.2] was recorded in single rat aorta and tail artery myocytes by the patch-clamp technique. Docking at a 3D model of the rat, α1c central pore subunit of the Cav1.2 channel was simulated in silico. KEY RESULTS In rat aorta rings MuA, at concentrations ≤14.2 μM, increased 30 mM K+-induced tone and shifted the concentration-response curve to K+ to the left. Conversely, at concentrations >14.2 μM, it relaxed high K+ depolarized rings and antagonized Bay K 8644- induced contraction. In single myocytes, MuA stimulated IBa1.2 in a concentration-dependent, bell-shaped manner; stimulation was stable, incompletely reversible upon drug washout and accompanied by a leftward shift of the voltage-dependent activation curve. MuA docked at the α1C subunit central pore differently from nifedipine and Bay K 8644, although apparently interacting with the same amino acids of the pocket. Neither Bay K 8644-induced stimulation nor nifedipine-induced block of IBa1.2 was modified by MuA. CONCLUSIONS AND IMPLICATIONS Murrayafoline A is a naturally occurring vasoactive agent able to modulate Cav1.2 channels and dock at the α1C subunit central pore in a manner that differed from that of dihydropyridines
    Article · Jan 2016 · British Journal of Pharmacology
  • [Show abstract] [Hide abstract] ABSTRACT: BACKGROUND AND PURPOSE - Annexin A6 (AnxA6) is a calcium-dependent phospholipid-binding protein that can be recruited to the plasma membrane to function as a scaffolding protein to regulate signal complex formation, endo- and exocytic pathways as well as distribution of cellular cholesterol. Here, we have investigated how AnxA6 influences the membrane order. EXPERIMENTAL APPROACH - We used Laurdan and di-4-ANEPPDHQ staining in (i) artificial membranes; (ii) live cells to investigate membrane packing and ordered lipid phases; and (iii) a super-resolution imaging (photoactivated localization microscopy, PALM) and Ripley’s K second-order point pattern analysis approach to assess how AnxA6 regulates plasma membrane order domains and protein clustering. KEY RESULTS - In artificial membranes, purified AnxA6 induced a global increase in membrane order. However, confocal microscopy using di-4-ANEPPDHQ in live cells showed that cells expressing AnxA6, which reduces plasma membrane cholesterol levels and modifies the actin cytoskeleton meshwork, displayed a decrease in membrane order (∼15 and 30% in A431 and MEF cells respectively). PALM data from Lck10 and Src15 membrane raft/non-raft markers revealed that AnxA6 expression induced clustering of both raft and non-raft markers. Altered clustering of Lck10 and Src15 in cells expressing AnxA6 was also observed after cholesterol extraction with methyl-β-cyclodextrin or actin cytoskeleton disruption with latrunculin B. CONCLUSIONS AND IMPLICATIONS - AnxA6-induced plasma membrane remodelling indicated that elevated AnxA6 expression decreased membrane order through the regulation of cellular cholesterol homeostasis and the actin cytoskeleton. This study provides the first evidence from live cells that support current models of annexins as membrane organizers.
    Article · Apr 2015 · British Journal of Pharmacology
  • [Show abstract] [Hide abstract] ABSTRACT: Endothelin (ET) receptor antagonism reduces neointimal lesion formation in animal models. This investigation addressed the hypothesis that the selective ETA receptor antagonist sitaxentan would be more effective than mixed ETA/B antagonism at inhibiting neointimal proliferation in a mouse model of intra-luminal injury. Antagonism of ETA receptors by sitaxentan (1-100nM) was assessed in femoral arteries isolated from adult, male C57Bl6 mice (25-35g) using isometric wire myography. Neointimal lesion development was induced by intraluminal injury in mice receiving sitaxentan (ETA antagonist; 15mg/kg/day), A192621 (ETB antagonist; 30 mg/kg/day), the combination of both antagonists, or vehicle (n=6-16). Treatment began one week before, and continued for 28 days after, surgery. Femoral arteries were then harvested for analysis of lesion size and composition. Sitaxentan produced a selective, concentration-dependent parallel rightward shift of ET-1-mediated contraction (pD2 ; 8.2±0.1 Control vs 7.2±0.1 100nM sitaxentan; P<0.001) in isolated femoral arteries. Sitaxentan reduced neointimal lesion size (23±5% vs 51±4%; P<0.05), whereas ETB (A192621; 61±7%) and combined ETA/B antagonism (51±7% P>0.05) did not. Macrophage and α-smooth muscle actin content were unaltered by ET antagonism but sitaxentan reduced the amount of collagen in lesions (14±2% vs 44±6%; p<0.01). These results suggest that ETA antagonism would be more effective than combined ETA / ETB antagonism at reducing neointimal lesion formation. This article is protected by copyright. All rights reserved.
    Article · Jan 2015 · British Journal of Pharmacology
  • [Show abstract] [Hide abstract] ABSTRACT: Antipsychotic drugs have been shown to modulate the expression of ATP-binding cassette transporter A1 (ABCA1), a key factor in the anti-atherogenic reverse cholesterol transport process, in vitro. Here we evaluated the potential of the typical antipsychotic drug haloperidol to modulate the macrophage cholesterol efflux function in vitro and susceptibility to atherosclerosis in vivo. Thioglycollate-elicited peritoneal macrophages were used for in vitro studies. Hyperlipidemic low-density lipoprotein (LDL) receptor knockout mice were implanted with a haloperidol-containing pellet and subsequently fed a Western-type diet for 5 weeks to induce the development of atherosclerotic lesions in vivo. Haloperidol induced a 54% decrease (P=0.043) in the mRNA expression of ABCA1 in peritoneal macrophages. This coincided with a 30% (P<0.001) decrease in the capacity of macrophages to efflux cholesterol to apolipoprotein A1. Haloperidol treatment stimulated the expression of ABCA1 (+51%; P=0.021) and other genes involved in reverse cholesterol transport, i.e. CYP7A1 (+98%; P=0.004) in livers of LDL receptor knockout mice. No change in splenic ABCA1 expression was noted. However, the average atherosclerotic lesion size was significantly smaller (-31%; P=0.039) in the context of a mildly more atherogenic metabolic phenotype upon haloperidol treatment. Importantly, haloperidol markedly lowered MCP-1 expression (-70%; P<0.001) and secretion (-28%; P=0.018) by peritoneal macrophages. These studies show that haloperidol treatment lowers the susceptibility for atherosclerotic lesion development in hyperlipidemic LDL receptor knockout mice. Our findings suggest that the beneficial effect on atherosclerosis susceptibility can be attributed to a haloperidol-induced inhibition of macrophage chemotaxis. This article is protected by copyright. All rights reserved.
    Article · Jan 2015 · British Journal of Pharmacology
  • [Show abstract] [Hide abstract] ABSTRACT: Background and purpose: Pancreatic cancer is characterized by alterations in several key signalling proteins, including increased expression and activity of the Src tyrosine kinase and focal adhesion kinase (FAK), which have been linked to its chemoresistance. Sustained Src inhibition reactivates survival pathways regulated by the transcription factor STAT3, also leading to resistance. Therefore, simultaneously targeting Src/FAK and STAT3 signalling could provide an important strategy for treating pancreatic cancer. Recently, we described novel quinazolinediones that increased generation of reactive oxygen species (ROS) and were cytotoxic in pancreatic cancer cells. Here, we have investigated effects of our lead compound, QD232, on Src/FAK and STAT3 signalling. Experimental approach: The major signalling pathways affected by QD232 in pancreatic cancer cell lines were identified by Kinexus proteomic analysis. Changes in key signalling proteins were confirmed by Western blotting. Cell migration was assessed by Boyden chamber and wound healing assays. Direct inhibition of kinase activity in vitro was assayed with a panel of 92 oncogenic kinases. Safety and efficacy of QD232 were determined in a xenograft mouse model of pancreatic cancer. Key results: QD232 potently inhibited Src/FAK and STAT3 phosphorylation, decreasing pancreatic cancer cell viability and migration. Furthermore, QD232 arrested cell cycle progression and induced apoptosis in these cells at low micromolar concentrations. Effects of QD232 on Src/FAK and STAT3 phosphorylation were blocked by N-acetylcysteine or glutathione. Conclusions and implications: QD232 is a novel compound with a unique, ROS-dependent mechanism, effective in drug-resistant cancer cell lines. This compound shows potential as therapy for pancreatic cancer.
    Article · Jan 2015 · British Journal of Pharmacology