Alison Gurney

Last updated
Professor Alison M. Gurney
Born1957
Alma mater
Known for
  • Mechanisms of ganglion block
  • Identification of ion channels regulating membrane potential in vascular smooth muscle
  • Mechanisms of vasodilation
Scientific career
Fields
Institutions
Thesis Effects of methonium compounds on rat submandibular ganglion cells  (1982)
Doctoral advisor Humphrey Rang [1] [2]
Other academic advisorsHenry Lester [3]
    Website Official website

    Alison Marion Gurney (born 1957) is professor of Pharmacology at the University of Manchester. She previously held the W.C. Bowman [4] Chair of Pharmacology at the University of Strathclyde, where she was the first female appointed to a science professorship and the first female Professor of Pharmacology in Scotland. She is known for her research into the pharmacology and physiological roles of ion channels, especially in the pulmonary circulation.

    Contents

    Education

    Gurney was educated at Prestwick Academy before attending the University of Aberdeen, where she graduated with a BSc degree in Pharmacology in 1979, then University College London, where she obtained a PhD in Pharmacology under the supervision of Professor Humphrey Rang. Together they identified a novel mechanism by which drugs that block neurotransmission across autonomic ganglia interact with neuronal nicotinic receptors.

    Career and research

    In 1982, Gurney moved to California to carry out postdoctoral research with Henry Lester at the California Institute of Technology, making use of novel light-sensitive compounds to study the interactions between drugs and receptors. She returned to the UK in 1985 to take up a lectureship in pharmacology at the United Medical and Dental Schools of Guy's and St Thomas's hospitals (now part of King's College), where she established a laboratory investigating ion channels in the cardiovascular system as a target for drugs to treat cardiovascular disease. While there she identified a positive feedback effect of cytoplasmic Ca2+ on cardiac calcium channels, [5] a role for ATP-sensitive potassium channels in regulating the membrane potential of artery smooth muscle cells [6] and the main features of the ion channels that set the resting potential of pulmonary artery smooth muscle cells. [7]

    After 10 years in London, Gurney moved to Glasgow to take up the W.C. Bowman Chair of Pharmacology at the University of Strathclyde. For the next 10 years she continued studying the pulmonary circulation, identifying key roles for store-operated SOC channels [8] and the two-pore-domain potassium channel TASK-1 [9] in regulating pulmonary artery tone and in the development of pulmonary hypertension. Along with physicists Allister Ferguson and John Girkin, she founded the Centre for Biophotonics and acted as its Director for the next 5 years. [10] In 2005, Gurney moved to the University of Manchester, where she continues to study ion channels in pulmonary artery disease, identifying KCNQ channels [11] as a possible biological target for drugs to treat pulmonary hypertension.

    Recognition

    Gurney was awarded the British Pharmacological Society Sandoz prize for her research in pharmacology in 1991, the Royal Pharmaceutical Society of Great Britain Conference Science Medal in 1992 and a Royal Society Leverhulme Trust Senior Research Fellowship in 2002.

    One of Gurney's papers, "The channel-blocking action of methonium compounds on rat submandibular ganglion cells" [12] was recognised in "Landmarks in Pharmacology", [13] a collection of the most significant papers published by the British Journal of Pharmacology during its first 50 years.

    Related Research Articles

    <span class="mw-page-title-main">Ion channel</span> Pore-forming membrane protein

    Ion channels are pore-forming membrane proteins that allow ions to pass through the channel pore. Their functions include establishing a resting membrane potential, shaping action potentials and other electrical signals by gating the flow of ions across the cell membrane, controlling the flow of ions across secretory and epithelial cells, and regulating cell volume. Ion channels are present in the membranes of all cells. Ion channels are one of the two classes of ionophoric proteins, the other being ion transporters.

    <span class="mw-page-title-main">Adrenergic receptor</span> Class of G protein-coupled receptors

    The adrenergic receptors or adrenoceptors are a class of G protein-coupled receptors that are targets of many catecholamines like norepinephrine (noradrenaline) and epinephrine (adrenaline) produced by the body, but also many medications like beta blockers, beta-2 (β2) agonists and alpha-2 (α2) agonists, which are used to treat high blood pressure and asthma, for example.

    <span class="mw-page-title-main">Systole</span> Part of the cardiac cycle when a heart chamber contracts

    Systole is the part of the cardiac cycle during which some chambers of the heart contract after refilling with blood.

    <span class="mw-page-title-main">Smooth muscle</span> Involuntary non-striated muscle

    Smooth muscle is an involuntary non-striated muscle, so-called because it has no sarcomeres and therefore no striations. It is divided into two subgroups, single-unit and multiunit smooth muscle. Within single-unit muscle, the whole bundle or sheet of smooth muscle cells contracts as a syncytium.

    <span class="mw-page-title-main">Vasoconstriction</span> Narrowing of blood vessels due to the constriction of smooth muscle cells

    Vasoconstriction is the narrowing of the blood vessels resulting from contraction of the muscular wall of the vessels, in particular the large arteries and small arterioles. The process is the opposite of vasodilation, the widening of blood vessels. The process is particularly important in controlling hemorrhage and reducing acute blood loss. When blood vessels constrict, the flow of blood is restricted or decreased, thus retaining body heat or increasing vascular resistance. This makes the skin turn paler because less blood reaches the surface, reducing the radiation of heat. On a larger level, vasoconstriction is one mechanism by which the body regulates and maintains mean arterial pressure.

    <span class="mw-page-title-main">Vasodilation</span> Widening of blood vessels

    Vasodilation, also known as vasorelaxation, is the widening of blood vessels. It results from relaxation of smooth muscle cells within the vessel walls, in particular in the large veins, large arteries, and smaller arterioles. The process is the opposite of vasoconstriction, which is the narrowing of blood vessels.

    <span class="mw-page-title-main">Potassium channel</span> Ion channel that selectively passes K+

    Potassium channels are the most widely distributed type of ion channel found in virtually all organisms. They form potassium-selective pores that span cell membranes. Potassium channels are found in most cell types and control a wide variety of cell functions.

    Vasospasm refers to a condition in which an arterial spasm leads to vasoconstriction. This can lead to tissue ischemia and tissue death (necrosis). Cerebral vasospasm may arise in the context of subarachnoid hemorrhage. Symptomatic vasospasm or delayed cerebral ischemia is a major contributor to post-operative stroke and death especially after aneurysmal subarachnoid hemorrhage. Vasospasm typically appears 4 to 10 days after subarachnoid hemorrhage.

    Hypoxic pulmonary vasoconstriction (HPV), also known as the Euler-Liljestrand mechanism, is a physiological phenomenon in which small pulmonary arteries constrict in the presence of alveolar hypoxia. By redirecting blood flow from poorly-ventilated lung regions to well-ventilated lung regions, HPV is thought to be the primary mechanism underlying ventilation/perfusion matching.

    <span class="mw-page-title-main">Hexamethonium</span> Chemical compound

    Hexamethonium is a non-depolarising ganglionic blocker, a neuronal nicotinic (nAChR) receptor antagonist that acts in autonomic ganglia by binding mostly in or on the nAChR receptor, and not the acetylcholine binding site itself. It does not have any effect on the muscarinic acetylcholine receptors (mAChR) located on target organs of the parasympathetic nervous system, nor on the nicotinic receptors at the skeletal neuromuscular junction, but acts as antagonist at the nicotinic acetylcholine receptors located in sympathetic and parasympathetic ganglia (nAChR).

    <span class="mw-page-title-main">Nicorandil</span> Chemical compound

    Nicorandil is a vasodilator drug used to treat angina.

    alpha-1 (α1) adrenergic receptors are G protein-coupled receptors (GPCRs) associated with the Gq heterotrimeric G protein. α1-adrenergic receptors are subdivided into three highly homologous subtypes, i.e., α1A-, α1B-, and α1D-adrenergic receptor subtypes. There is no α1C receptor. At one time, there was a subtype known as α1C, but it was found to be identical to the previously discovered α1A receptor subtype. To avoid confusion, naming was continued with the letter D. Catecholamines like norepinephrine (noradrenaline) and epinephrine (adrenaline) signal through the α1-adrenergic receptors in the central and peripheral nervous systems. The crystal structure of the α1B-adrenergic receptor subtype has been determined in complex with the inverse agonist (+)-cyclazosin.

    <span class="mw-page-title-main">TRPC6</span> Protein and coding gene in humans

    Transient receptor potential cation channel, subfamily C, member 6 or Transient receptor potential canonical 6, also known as TRPC6, is a human gene encoding a protein of the same name. TRPC6 is a transient receptor potential channel of the classical TRPC subfamily.

    <span class="mw-page-title-main">Prostacyclin receptor</span> Mammalian protein found in Homo sapiens

    The Prostacyclin receptor, also termed the prostaglandin I2 receptor or just IP, is a receptor belonging to the prostaglandin (PG) group of receptors. IP binds to and mediates the biological actions of prostacyclin (also termed Prostaglandin I2, PGI2, or when used as a drug, epoprostenol). IP is encoded in humans by the PTGIR gene. While possessing many functions as defined in animal model studies, the major clinical relevancy of IP is as a powerful vasodilator: stimulators of IP are used to treat severe and even life-threatening diseases involving pathological vasoconstriction.

    <span class="mw-page-title-main">Calcium-activated potassium channel subunit alpha-1</span> Voltage-gated potassium channel protein

    Calcium-activated potassium channel subunit alpha-1 also known as large conductance calcium-activated potassium channel, subfamily M, alpha member 1 (KCa1.1), or BK channel alpha subunit, is a voltage gated potassium channel encoded by the KCNMA1 gene and characterized by their large conductance of potassium ions (K+) through cell membranes.

    <span class="mw-page-title-main">KCNB1</span> Protein-coding gene in the species Homo sapiens

    Potassium voltage-gated channel, Shab-related subfamily, member 1, also known as KCNB1 or Kv2.1, is a protein that, in humans, is encoded by the KCNB1 gene.

    <span class="mw-page-title-main">KCNJ12</span> Protein-coding gene in the species Homo sapiens

    ATP-sensitive inward rectifier potassium channel 12 is a lipid-gated ion channel that in humans is encoded by the KCNJ12 gene.

    <span class="mw-page-title-main">KCNS3</span> Protein-coding gene in the species Homo sapiens

    Potassium voltage-gated channel subfamily S member 3 (Kv9.3) is a protein that in humans is encoded by the KCNS3 gene. KCNS3 gene belongs to the S subfamily of the potassium channel family. It is highly expressed in pulmonary artery myocytes, placenta, and parvalbumin-containing GABA neurons in brain cortex. In humans, single-nucleotide polymorphisms of the KCNS3 gene are associated with airway hyperresponsiveness, whereas decreased KCNS3 mRNA expression is found in the prefrontal cortex of patients with schizophrenia.

    A potassium channel opener is a type of drug which facilitates ion transmission through potassium channels.

    <span class="mw-page-title-main">Colin Nichols</span> English academic

    Colin G. Nichols FRS is the Carl Cori Endowed Professor, and Director of the Center for Investigation of Membrane Excitability Diseases at Washington University in St. Louis, Missouri.

    References

    1. "Humphrey Rang | Royal Society". royalsociety.org.
    2. "Rang & Dale's Pharmacology - 9780702074486 | Elsevier Health - UK". www.uk.elsevierhealth.com.
    3. "Dr Henry A Lester | Lester Research Group". lester.caltech.edu.
    4. "Bio" (PDF). www.rse.org.uk. Retrieved 2020-05-20.
    5. Gurney, A. M.; Charnet, P.; Pye, J. M.; Nargeot, J. (September 1989). "Augmentation of cardiac calcium current by flash photolysis of intracellular caged-Ca 2+ molecules". Nature. 341 (6237): 65–68. Bibcode:1989Natur.341...65G. doi:10.1038/341065a0. ISSN   1476-4687. PMID   2549428. S2CID   4268164.
    6. Clapp, L. H.; Gurney, A. M. (1992-03-01). "ATP-sensitive K+ channels regulate resting potential of pulmonary arterial smooth muscle cells". American Journal of Physiology. Heart and Circulatory Physiology. 262 (3): H916–H920. doi:10.1152/ajpheart.1992.262.3.H916. ISSN   0363-6135. PMID   1558201.
    7. Evans, A. M.; Osipenko, O. N.; Gurney, A. M. (1996). "Properties of a novel K+ current that is active at resting potential in rabbit pulmonary artery smooth muscle cells". The Journal of Physiology. 496 ( Pt 2) (2): 407–20. doi:10.1113/jphysiol.1996.sp021694. PMC   1160886 . PMID   8910225.
    8. Ng Lih Chyuan; Gurney Alison M. (2001-11-09). "Store-Operated Channels Mediate Ca2+ Influx and Contraction in Rat Pulmonary Artery". Circulation Research. 89 (10): 923–929. doi: 10.1161/hh2201.100315 . PMID   11701620.
    9. Gurney, A.M.; Osipenko, O.N.; MacMillan, D.; McFarlane, K.M.; Tate, R.J.; Kempsill, F.E.J. (2003). "Two-Pore Domain K Channel, TASK-1, in Pulmonary Artery Smooth Muscle Cells". Circulation Research. 93 (10): 957–964. doi: 10.1161/01.res.0000099883.68414.61 . PMID   14551239.
    10. "Prof JM Girkin - Durham University". www.dur.ac.uk. Retrieved 2020-04-14.
    11. Gurney, Alison M.; Joshi, Shreena; Manoury, Boris (2010). Yuan, Jason X. -J.; Ward, Jeremy P. T. (eds.). "KCNQ Potassium Channels: New Targets for Pulmonary Vasodilator Drugs?". Membrane Receptors, Channels and Transporters in Pulmonary Circulation. Advances in Experimental Medicine and Biology. Totowa, NJ: Humana Press. 661: 405–417. doi:10.1007/978-1-60761-500-2_26. ISBN   978-1-60761-500-2. PMID   20204745.
    12. Gurney, A.M.; Rang, H.P. (1997-02-01). "The channel-blocking action of methonium compounds on rat submandibular ganglion cells". British Journal of Pharmacology. 120 (S1): 471–490. doi:10.1111/j.1476-5381.1997.tb06837.x. ISSN   0007-1188. PMC   3224332 . PMID   9142425.
    13. Birmingham, A. T; Brown, D. A (1997). Landmarks in pharmacology: a selection from papers published in the British Journal of Pharmacology since its foundation in 1946. Hampshire [UK: MacMillan Press. ISBN   978-0-333-71930-5. OCLC   36960433.