Director of Human Receptor Research group
Fellow of St Catharine’s College, University of Cambridge.
One third of all currently used medicines target G-protein-coupled receptors (GPCRs) belonging to Class 1 or Family A, part of the ‘druggable genome’. The aim of our research is to understand the role of GPCRs, together with their transmitters in the human cardiovascular system and how these are altered with disease, in particular the consequences of endothelial cell dysfunction, to identify new targets for novel drugs.
The group is unusual in being able to compare responses in diseased versus normal human tissues which can be maintained in organ baths for several hours. Using tissues obtained with ethical approval and informed consent at the time of surgery, we measure responses to chemical messengers such as endothelin-1 (ET-1), novel transmitters or drugs as changes in vascular reactivity or the force of contraction of the heart. We focus on discovering the role in humans of novel ‘orphan’ GPCRs, originally predicted to exist from the human genome but recently paired with their cognate transmitters. Using this approach, we have characterized GPCRs expressed in the human cardiovascular system and identified a novel cardiovacular role for transmitters including apelin, chemokines and kisspeptins.
Discovery of biased apelin receptor agonist, MM07 and first in human studies
The peptide apelin is the endogenous ligand for a novel G-protein coupled receptor with an emerging key role in cardiovascular disease. Apelin is the most potent positive inotropic agent discovered in human hearts, and an endothelium-dependent vasodilators in human vessels (Hypertension).
The apelin signalling pathway is downregulated in human pulmonary arterial hypertension (PAH). Animal studies suggest that the development of PAH can be attenuated by infusion of apelin but to date no apelin agonists have been developed for clinical use. We hypothesise that a first in class agonist is required to activate the apelin receptor in PAH to replace the missing peptide. However, a potential limitation of GPCR agonists, is they can desensitise target receptors by recruiting the β-arrestin pathway and internalization (Trends in Pharmacology.)
With Robert Glen (Department of Chemistry, University of Cambridge) we discovered MM07, a novel cyclical apelin analogue that is biased towards the desirable G-protein pathway but two orders of magnitude less effective at recruiting the β-arrestin pathway and internalization. In first in human, proof of principle studies, MM07 was a more efficacious dilator in human forearm and hand vein via the G-protein mediated pathway than the endogenous peptides. On repeated dosing, there was no evidence of desensitisation. Following systemic infusion in rats a significant increase in cardiac output was observed without any change in heart rate or blood pressure. These results are consistent with MM07 functioning as an agonist biased to the G-protein pathway, with reduced arrestin recruitment and internalization.
Cardiac action of the first G protein biased small molecule apelin agonist.
We have demonstrated that G protein over β-arrestin/internalisation bias can be retained in a non-peptide small molecule with drug like properties, CMF-019. CMF-019 caused a significant increase in cardiac contractility in vivo without desensitising the apelin receptor. CMF-019 is suitable as a tool compound and provides the basis for design of biased agonists with improved pharmacokinetics for treatment of cardiovascular conditions such as PAH (Biochemical Pharmacology).
First in human studies show [Pyr1]Apelin-131-12 is a biologically active ACE-2 metabolite of [Pyr1]apelin-13
[Pyr1]apelin-13 is the predominant isoform in the human cardiovascular system and is a predicted substrate for angiotensin converting enzyme-2 (ACE-2). Recombinant ACE-2 is a novel therapeutic agent (APN01) in phase II clinical trials for acute lung injury. We have shown that ACE2 cleaves [Pyr1]apelin-13 to [Pyr1]Apelin-131-12 and this cleavage product is expressed in human cardiovascular tissues. In first in human studies, we found the metabolite retained the desirable vasodilator properties of the parent molecule, rather than being inactivated as predicted from studies in animals. These results are important since recombinant ACE-2 in a clinical setting would be expected to convert the native peptide to [Pyr1]Apelin-131-12 but importantly still retain biological activity. (Frontiers in Neuroscience)
The first competitive apelin receptor antagonist, MM54 was discovered in collaboration with Robert Glen (Department of Chemistry, University of Cambridge (ChemMedChem). Dr Julie Gavard (University of Nantes) and colleagues, have shown MM54 has remarkable anti-cancer properties in models of glioblastoma. Glioblastoma are highly aggressive brain tumours and are associated with increased levels of apelin. Despite surgery, radiation and chemotherapy, outcomes remain poor and there is an unmet need for better therapies. Apelin antagonists appear to suppress endothelial-mediated expansion of glioblastoma patient-derived cells with stem-like properties and suppresses tumour initiation and growth. MM54 increased the survival of intracranially xenografted mice and was synergistic with the standard of care therapy, temozolomide (Brain, 2017).
Elabela/Toddler: Fish peptide treats cardiovascular disease (Circulation)
We have shown a new peptide, Elabela/Toddler (ELA), first identified in the fish Danio as critical for the development of the heart, is also present in the human cardiovascular system
ELA binds to the apelin receptor in human heart and downstream signaling is blocked by the apelin receptor antagonists, MM54
In vivo, ELA increased cardiac contractions visulised below in transverse section by magnetic resonance imaging. Importantly, we found that like apelin, ELA expression was reduced in patients with PAH. However, daily injections of ELA to replace the missing peptide, attenuated the development of PAH in an animal model of this disease, suggesting a potential target for translational research.
Endothelin-1 (ET-1) is the principal isoform in the human cardiovascular system ETs mediate their action by activating two G protein-coupled receptors, ETA and ETB. ET-3 is the only isoform that distinguishes between the two receptors, having the same affinity at the ETB receptor as ET-1 but at physiological concentrations, has little or no affinity for the ETA (Pharmacological Review)
We have discovered that ET-1 is unusual among the mammalian bioactive peptides in being released from a dual secretory pathway. The peptide is continuously released from endothelial cells by the constitutive pathway, contributing to the maintenance of vascular tone. ET-1 is also released from endothelial cell-specific storage granules (Weibel-Palade bodies, WP) in response to external physiological, or pathophysiological stimuli producing further vasoconstriction. Thus, ET-1 functions as a locally released, rather than circulating, hormone. In humans, ETA receptors predominate in the medial layer of vessels but the low density of ETB receptors (<15%) contributes little to vasoconstriction in either normal or importantly, diseased tissue. In human isolated vessels, ETA selective antagonists can fully reverse ET-1 mediated constriction(Circulation Research, 1993,1996,1998,1999,Stroke,1999).
In contrast, in vivo positron emission tomography imaging using the first 18F-labelled endothelin-1 and 18F-big-endothelin-1 ligands to be synthesized, revealed the importance of ETB receptors, clearing endothelin-1 from the circulation thus protecting the heart from detrimental elevated levels of peptide. (BJP,2006,2010). ETB receptors present on endothelial cells mediate the beneficial release of endothelium-derived relaxing factors including nitric oxide and prostanoids. High densities of ETB receptors are present in lung, kidney and liver, where this sub-type functions as a clearing receptor, to internalize and remove ET from the circulation. This differential cellular localization in humans provides the rationale that ETA selective compounds could have a therapeutic benefit by blocking ETA mediated vasoconstriction but sparing ETB mediated vasodilatation and clearing from the circulation.
Imaging atherosclerotic calcification or ‘hardening of the arteries’ using 18F-NaF positron emission tomography (Nature Communications)
Atherosclerosis (or ‘hardening of the arteries’) is a potentially serious condition where arteries become clogged with one of the key components being deposits of calcium. In some people, pieces from the calcified artery can break away – if the artery supplies the brain or heart, this can lead to stroke or heart attac. We have shown how a radioactive agent developed in the 1960’s to detect bone cancer can be re-purposed to highlight the build-up of unstable calcium deposits in arteries. Sodium fluoride tagged with a tiny amount of radioactivity (18F-NaF), was infused into patients in the clinic and the progress of the radiotracer around the body followed using a combined positron emission tomography(PET)/ computed tomography (CT) scanner to give a three dimensional image of the calcified lesion. In the same way that sodium fluoride in toothpaste binds to calcium hydroxyapatite in teeth, 18F-NaF binds to areas of calcification in carotid arteries. Following their 18F-NaF scans, the patients had surgery to remove calcified plaques and the extracted tissue was imaged, this time at higher resolution, using a laboratory PET/CT scanner and an electron microscope. This confirmed that the radiotracer accumulates in areas of active, unstable calcification whilst avoiding surrounding tissue. Sodium fluoride is a simple and inexpensive radiotracer that that has the potential to revolutionise the detection of dangerous calcium in the arteries of the heart and brain and to make current treatments more effective by giving them to those patients at highest risk.
International Union of Pharmacology Committee on Receptor Nomenclature and Drug Classification (NC-IUPHAR)
The group contributes to NC-IUPHAR http://www.guidetopharmacology.org/nciuphar.jsp to curate an expert-driven guide to pharmacological targets and drug classification database GuidetoPharmacology http://www.guidetopharmacology.org/ and the Concise Guide To Pharmacology G Protein-Coupled Receptors. http://onlinelibrary.wiley.com/doi/10.1111/bph.13878/epdf
BHF 4-year PhD Studentship Programme in Cardiovascular Research
Dr Anthony Davenport is a participating investigator and Programme Co-ordinator (Laboratory Stream) in this British Heart Foundation funded PhD programme:. https://www.cardiovascular.cam.ac.uk/students/prospective/phd-bhfcardio
This exciting programme is a new initiative for scientists to carry out cross-disciplinary cardiovascular research, combining training in molecular and cellular biology, physiology of model organisms, human pharmacology physiology, genetics, genomics and population health sciences. The programme will operate with a 1+3 year structure. In the first year students will undertake three rotation projects to provide training in a broad range of scientific disciplines and techniques. In years 2-4, students will undertake a 3 year PhD project with a selected supervisor, strong encouragement being be given to the development of collaborative interdisciplinary reserach.
Applications open in the autumn with a closing date in early December. Further information can be found at: https://www.cardiovascular.cam.ac.uk/students/prospective/phd-bhfcardio/apply
Wellcome Trust 4-Year Studentship PhD Programme in Metabolic and Cardiovascular Disease
The Wellcome Trust Cambridge 4-year PhD programme has close links and shares many investigators with the BHF-funded 4-year PhD programme in Cardiovascular Research. Students interested in cardiovascular research in Cambridge can apply to both programmes using a single application form. Together these programmes will support around 8 students per year.
Applications open in the autumn with a closing date in early January. Further information can be found at:
Yang, P., Read, C., , Kuc, R.E., Buonincontri, G., Southwood, M., Torella, R., Upton, P.D., Crosby., A., Sawiak. S.J., Carpenter, T.A., Glen, R.C., Morrell, N.W., Maguire, J.J. and Davenport, A.P. (2017). Elabela/Toddler is an endogenous agonist of the apelin APJ receptor in the adult cardiovascular system, and exogenous administration of the peptide compensates for the downregulation of its expression in pulmonary arterial hypertension. Circulation, 135, 1160–1173. http://circ.ahajournals.org/content/135/12/1160.long
Yang, P., Kuc, R.E., Brame, A.L., Dyson, A., Singer, M., Glen, R.C., Cheriyan, J., Wilkinson, I.B., Davenport, A.P. and Maguire, J,J. (2017) [Pyr1]Apelin-13(1-12) is a biologically Active ACE2 Metabolite of the Endogenous Cardiovascular Peptide [Pyr1] Apelin-13. Frontiers in Neuroscience. 1-14. https://www.frontiersin.org/articles/10.3389/fnins.2017.00092/full
Harford-Wright, E., Andre-Gregoire, G., Jacobs, K.A., Treps, L., Le Gonidec, S., Leclair, H.M., Gonzalez-Diest, S., Roux, Q., Guillonneau, F, Loussouarn, D., Oliver, L., Vallette, F.M., Foufelle, F., Valet, P., Davenport, A.P., Glen, R.C., Bidere, N. and Gavard, J. (2017) Targeting glioma cell self-renewal and tumourigenicity through pharmacological blockade of apelin. Brain, 140, 1-16.
Tarkin, J.M., Joshi, F.R., Evans,, N.R., Chowdhury M.M., Figg, N.L., Shah, A.V., Starks, L.T., Martin-Garrido, A., Manavaki, R, Yu, E, Kuc, R.E., Grassi, L., Kreuzhuber, R., Kostadima, M.A., Frontini, M., Kirkpatrick, P.J., Coughlin, P.A, Gopalan, D., Fryer, T.D., Buscombe, J.R., Groves, A.M., Ouwehand, W.H., Bennett,. M.R., Warburton E.A., Davenport, A.P., Rudd, J.H. (2017). Detection of Atherosclerotic Inflammation by (68)Ga-DOTATATE PET Compared to [18F]FDG PET Imaging. Journal of the American College of Cardiology, 69, 1774-1791. http://www.sciencedirect.com/science/article/pii/S0735109717306927?via%3Dihub
Joshi, F. R., Manavaki, R., Fryer, T.D., Figg, N.L., Sluimer, J.C., Aigbirhio, F.I., Davenport, A.P., Kirkpatrick, P.J., Warburton, E.A., Rudd, J.H. (2017) Vascular Imaging With 18F-Fluorodeoxyglucose Positron Emission Tomography Is Influenced by Hypoxia. Journal of American College of Cardiology, 69, 1873-1874. http://www.sciencedirect.com/science/article/pii/S0735109717305624?via%3Dihub
Vesey, A.T. , Jenkins, W.S.A, Irkle, A, Moss A., Sng G., Forsythe, R.O., Clark, T., Roberts, G., Fletcher, A., Lucatelli, C. Rudd, J., Davenport, A.P., Mills, N.L., Al-Shahi Salman, R, Dennis, M. Whiteley, W. van Beek, E.J.R., Dweck, M.R. and Newby, D.E. (2017) 18F-Fluoride and 18F-fluorodeoxyglucose positron emission tomography after transient ischemic attack or minor ischemic stroke: case-control study. Circulation Cardiovascular Imaging. 10, 1-9 doi: 10.1161/CIRCIMAGING.116.004976. http://circimaging.ahajournals.org/content/10/3/e004976.long
Kennedy, A.J., Yang, P., Read, C., Kuc, R.E., Yang, L., Taylor, E.J.A., Taylor, C.W., Maguire, J.J. and Davenport, A.P. (2016) Chemerin Elicits Potent Constrictor Actions via CMKLR1, not GPR1, in Human and Rat Vasculature. Journal of the American Heart Association, 1-14 DOI 10.1161/JAHA.116.004421). http://jaha.ahajournals.org/content/5/10/e004421.long
Read, C., Fitzpatrick, C.M., Yang, P., Kuc, R.E., Maguire, J.J., Glen, R.C., Foster, R.E., Davenport, A.P. (2016) Cardiac action of the first G protein biased small molecule apelin agonist. Biochemical Pharmacology, 116, 63-72. http://www.sciencedirect.com/science/article/pii/S0006295216301952?via%3Dihub
Southwood, M., Ross, R.V., Kuc, R.E., Hagan, G., Sheares, K.K., Jenkins, D.P., Goddard, M., Davenport, A.P., Pepke-Zaba J. (2016) Endothelin ETA receptors predominate in chronic thromboembolic pulmonary hypertension. Life Sciences, 159, 104-10. http://www.sciencedirect.com/science/article/pii/S0024320516300868?via%3Dihub
Jiang, H., Salmon, R.M., Upton, P.D., Wei, Z., Lawera, A., Davenport, A.P., Morrell, N.W., Li, W.(2016) The Prodomain-Bound Form of Bone Morphogenetic Protein 10 is Biologically Active on Endothelial Cells. Journal of Biological Chemistry, 291; 2954-2966. http://www.jbc.org/content/291/6/2954.long
Irkle, A., Vesey, A.T., Lewis; D.Y., Skepper, J.N., Bird; J.L.E., Dweck; M.R., Joshi; F.R., Gallagher; F.A., Warburton; E.A., Bennett; M.R., Brindle; K.M., Newby, D.E., Rudd, J.H., Davenport, A.P. (2015) Identifying active vascular micro-calcification by 18F-sodium fluoride positron emission tomography. Nature Communications, 6:7495 1-11. http://www.nature.com/articles/ncomms8495
Haris Shaikh, L., Zhou, J., , Teo, A.E.D., Garg, S., Azizan, E.A.B., Neogi, S.G., McFarlane, I, De Vera Mudry, M.C., Nichola Figg4, Giles S Yeo5, Haixiang Yu4, Janet J. Maguire1, Wanfeng, Z., Bennett, M.R., Davenport, A.P., McKenzie, G. and Brown, M.J. (2015) LGR5 activates non-canonical Wnt-signaling and inhibits aldosterone production in the human adrenal”, Journal of Clinical Endocrinology and Metabolism, 100, E836–E844. https://academic.oup.com/jcem/article-lookup/doi/10.1210/jc.2015-1734
Brame, A.L., Maguire, J.J., Yang, BA, Dyson, A, Torella, R., Cheriyan, J., Singer, M., . Glen, R.C., Wilkinson, I.B., Davenport, A.P. (2015). Design, characterization and first-in-human study of the vascular actions of a novel ‘biased’ apelin receptor agonist. Hypertension, 65, 834-840. http://hyper.ahajournals.org/content/65/4/834.long
Cuhlmann S., Gsell W., Van der Heiden K., Habib J. Tremoleda J.L., Khalil M., Turkheimer F., Meens M.J., Kwak B.R., Bird J., Davenport, A. P., Clark J., Haskard D., Krams R., Jones H. and Evans P.C. (2014). In Vivo Mapping of Vascular Inflammation Using the Translocator Protein Tracer 18F-FEDAA1106. Molecular Imaging, 13, 1-10. http://journals.sagepub.com/doi/abs/10.2310/7290.2014.00014?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed&
Ooi C.Y., Sutcliffe, M.P., Davenport, A.P. and Maguire, J. J. (2014) Changes in biomechanical properties f the coronary artery wall contribute to maintained contractile responses to endothelin-1 in atherosclerosis. Life Sciences. 118, 424-429 http://www.sciencedirect.com/science/article/pii/S0024320514003816?via%3Dihub
Kuc R.E., Maguire, J.J., Siew, K., Patel, S., Derksen, D.R., V, M.Jackson, O’Shaughnessey K.M., Davenport, A.P. (2014) Characterization of [(125)I]GLP-1(9-36), a novel radiolabeled analog of the major metabolite of glucagon-like peptide 1 to a receptor distinct from GLP1-R and function of the peptide in murine aorta. Life Sciences 102, 134-138. http://www.sciencedirect.com/science/article/pii/S002432051400335X?via%3Dihub
Kuc, R.E., Carlebur, M., Maguire, J.J., Yang, P., Long, L., Toshner, M., Morrell, N.W. and Davenport, A.P. (2014). Modulation of endothelin receptors in the failing right ventricle of the heart and vasculature of the lung in human pulmonary arterial hypertension. Life Sciences. 118, 391-396. http://www.sciencedirect.com/science/article/pii/S0024320514002628?via%3Dihub
Maguire, J.J.,. Jones, K.L Kuc, R.E. Clarke, M.C.. Bennett, M.R and Davenport, A. P.. (2014). The CCR5 chemokine receptor mediates vasoconstriction and stimulates intimal hyperplasia in human vessels in vitro. Cardiovascular Research, 101, 513-21. https://academic.oup.com/cardiovascres/article-lookup/doi/10.1093/cvr/cvt333
Pawson, A.J.,. Sharman, J.L. Benson, H.E, Faccenda, E. Alexander, S.P. Buneman, O.P., Davenport, A.P., McGrath, J.C., Peters, J.A., Southan, C., Spedding, M., Yu, W. and Harmar. A.J. (2014). The IUPHAR/BPS Guide to PHARMACOLOGY: an expert-driven knowledgebase of drug targets and their ligands. Nucleic Acids Res 42: D1098-106. https://academic.oup.com/nar/article-lookup/doi/10.1093/nar/gkt1143
Astin, R.,. Bentham, R Djafarzadeh, S. Horscroft, J.A. Kuc, R.E. Leung, P.S. Skipworth, J.R. Vicencio, J.M. Davenport, A.P. Murray, A.J. Takala, J. Jakob, S.M. Montgomery, H. and Szabadkai G. (2013). No evidence for a local renin-angiotensin system in liver mitochondria. Sciences Rep 3: 2467. http://www.nature.com/articles/srep02467
Azizan, E.A., Poulsen, H.. Tuluc, P Zhou, J. Clausen M.VLieb, ., A. Maniero, C. Garg, S.. Bochukova E.G,. Zhao W. Shaikh, L.H,. Brighton C.A,. Teo A.E,. Davenport, A.P, Dekkers T., Tops B.,. Kusters B,. Ceral, J. Yeo G.S,. Neogi S.G, McFarlane I., N. Rosenfeld, F. Marass, J. Hadfield, W. Margas, K. Chaggar, M. Solar, J. Deinum, A.C. Dolphin, I.S. Farooqi, J. Striessnig, Nissen P., and. Brown. M.J (2013). Somatic mutations in ATP1A1 and CACNA1D underlie a common subtype of adrenal hypertension. Nature Genetics 45, 1055-1060. http://www.nature.com/ng/journal/v45/n9/full/ng.2716.html
Southern, C.,. Cook, J.M Neetoo-Isseljee Z.,. Taylor, D.L Kettleborough, C.A. Merritt, A.. Bassoni, D.L Raab W.J., Quinn, E.. Wehrman, T.S Davenport, A.P, Brown, A.J.. Green, A Wigglesworth M.J., and Rees S.. (2013). Screening beta-arrestin recruitment for the identification of natural ligands for orphan G-protein-coupled receptors. Journal of Biomolecular Screening 18, 599-609. http://journals.sagepub.com/doi/abs/10.1177/1087057113475480?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed
Sharman, J.L.,. Benson, H.E, Pawson, A.J., Lukito, V., Mpamhanga, C.P., Bombail, V., Davenport, A.P, Peters, J.A, Spedding, M. and Harmar, A.J.. (2013). IUPHAR-DB: updated database content and new features. Nucleic Acids Res 41: D1083-1088. https://academic.oup.com/nar/article-lookup/doi/10.1093/nar/gks960
Maguire; J. J., Kuc; R.E. and Davenport, A.P. (2012) Defining the affinity and receptor sub-type selectivity of four classes of endothelin antagonists in clinically relevant human cardiovascular tissues. Life Sciences 91, 681-686 http://www.sciencedirect.com/science/article/pii/S0024320512002676?via%3Dihub
Maguire, J.J., Kuc, R.E., Pell, V.R., Green, A., Kumar, M., Wehrman, T., Quinn E., Davenport, A.P. (2012). Comparison of human ETA and ETB receptor signalling via G-protein and β-arrestin pathways. Life Sciences ;91, 544-549. http://www.sciencedirect.com/science/article/pii/S0024320512001440?via%3Dihub
Seed, A., Kuc, R.E., Maguire, J.J., Hillier, C., Johnston, F., Essers, H., de Voogd, H.J., McMurray, J., Davenport, A. P. (2012). The dual endothelin converting enzyme/neutral endopeptidase inhibitor SLV-306 (daglutril), inhibits systemic conversion of big endothelin–1 in humans. Life Sciences ;91, 743-748. http://www.sciencedirect.com/science/article/pii/S0024320512001452?via%3Dihub
Ling, L., Kuc, R.E., Maguire, J.J., Davie, N.J., Webb, D.J., Gibbs, P., Alexander, G.J. M., Davenport, A.P. (2012). Comparison of endothelin receptors in normal versus cirrhotic human liver and in the liver from endothelial cell-specific ETB knockout mice. Life Sciences, 91, 716-722.http://www.sciencedirect.com/science/article/pii/S0024320512000665?via%3Dihub
Maguire JJ, Kirby HR, Mead EJ, Kuc RE, d’Anglemont de Tassigny X, Colledge WH, Davenport, A.P. (2011) Inotropic Action of the Puberty Hormone Kisspeptin in Rat, Mouse and Human: Cardiovascular Distribution and Characteristics of the Kisspeptin Receptor. PLoS ONE 6(11): e27601. doi:10.1371/journal.pone.0027601
Macaluso, N.J. M., Pitkin, S.L., Maguire, J.J., Davenport, A.P., Glen R.C. ChemMedChem (2011). Discovery of a competitive Apelin (APJ) receptor antagonist. ChemMedChemistry, 6, 1017-1023. http://onlinelibrary.wiley.com/doi/10.1002/cmdc.v6.6/issuetoc
Pitkin, S.L., Maguire, J.J., Kuc, R.E. and Davenport. A.P. (2010) Modulation of the apelin/APJ system in heart failure and atherosclerosis in man. British Journal of Pharmacology,160,1785-95. http://bpspubs.onlinelibrary.wiley.com/hub/issue/10.1111/bph.2010.160.issue-7/
Bird JL, Izquierdo-Garcia D, Davies JR, Rudd JH, Probst KC, Figg N, Clark JC, Weissberg PL, Davenport, A.P., Warburton EA..(2010) Evaluation of translocator protein quantification as a tool for characterising macrophage burden in human carotid atherosclerosis. Atherosclerosis, 210,388-391. http://www.nrcresearchpress.com/doi/abs/10.1139/Y10-041?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dwww.ncbi.nlm.nih.gov#.WgLog2eDM6s
166 Johnström P, Fryer TD, Richards HK, Clark JC, Pickard JD, Davenport, A.P. (2010). Positron emission tomography of [18F]-big endothelin-1 reveals renal excretion but tissue specific conversion to [18F]- endothelin-1 in lung and liver. British Journal of Pharmacology 159, 812-819. http://bpspubs.onlinelibrary.wiley.com/hub/issue/10.1111/bph.2010.159.issue-4/
Kelland., N.F., Kuc, R.E., McLean, D.L., Azfer, A., Bagnall, A.J., Gray, G.A., Gulliver-Sloan, F.H., Maguire, J.J., Davenport, A.P., Kotelevtsev, Y.V. and Webb, D.J. (2010). Endothelial Cell specific ETB receptor knockout: Autoradiographic and histological Characterisation and crucial role in the clearance of Endothelin-1. Canadian Journal of Physiology and Pharmacology, 88, 644-651. http://www.nrcresearchpress.com/doi/abs/10.1139/Y10-041?url_ver=Z39.88-003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dwww.ncbi.nlm.nih.gov#.WgLumGeDM6s
Davies, J.R., Izquierdo-Garcia, D, Rudd, J.H, Figg, N., Richards, H.K., Bird, J.L., Aigbirhio, F.I., Davenport, A.P. Weissberg, P.L., Fryer, T.D., Warburton, E.A. (2010). FDG-PET can distinguish inflamed from non-inflamed plaque in an animal model of atherosclerosis. International Journal of Cardiovascular Imaging, 26,41-48. https://link.springer.com/article/10.1007%2Fs10554-009-9506-6
Mitchell, J.D., Kuc, R.E., Maguire, J.J., Davenport, A.P. (2010). Evidence for a novel vasospastic transmitter system, neuromedin U, in the equine digital circulation. Veterinary Journal, 186,106-109. http://www.sciencedirect.com/science/article/pii/S1090023309002706?via%3Dihub
Maguire,J.J., Kleinz,M.J., Pitkin,S.L., Davenport, A.P.(2009) [Pyr1]apelin-13 identified as the predominant apelin isoform in human heart: vasoactive mechanisms and inotropic action in disease. Hypertension, 54:598-604). http://hyper.ahajournals.org/content/54/3/598.long
Editorials, Chapters and Reviews
Alexander, S.P., Kelly, E., Marrion, N.V., Peters, J.A., Faccenda, E., Harding, S.D., Pawson, A.J., Sharman, J.L., Southan, C., Buneman, O.P.,, Cidlowski, J.A., Christopoulos, A., Davenport, A.P., Fabbro, D., Spedding, M., Striessnig, J., Davies, J.A.; CGTP Collaborators (2017) THE CONCISE GUIDE TO PHARMACOLOGY 2017/18: Overview. Br J Pharmacol. 174 Suppl 1:S1-S16 http://bpspubs.onlinelibrary.wiley.com/hub/issue/10.1111/bph.v174.S1/
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