Dr Rich Rainbow

Patch Clamping

Lecturer in Cardiovascular Cell Physiology

Department of Cardiovascular Sciences
University of Leicester
Henry Wellcome Building
Lancaster Road
Leicester, LE1 9HN

Tel: +44 (0)116 229 7140

Email: rdr8@le.ac.uk

ORCID iD iconorcid.org/0000-0002-0532-1992


Personal details

  • BSc. (Medical Biochemistry), 1999, University Of Leicester
  • PhD. (Electrophysiology), 2003, University Of Leicester
  • Fellow of the Higher Education Academy,  2016

Membership of Learned Societies

  • The Physiological Society of the UK, 2001-present
  • The Biophysical Society, 2001-present
  • The American Heart Association, 2013-present

Current funding

  • British Heart Foundation Project Grant ('Understanding mechanisms of cardioprotection: The overlooked role of Kir6.1 in cardiac muscle') (in collaboration with Dr Caroline Dart, University of Liverpool)
  • The van Geest Cardiovascular Research Fund ('Development of a novel cardioprotective compound')
  • Leicester Drug Discovery and Diagnostics Centre ('Development of a novel cardioprotective compound')
  • Proof of Concept Fund (UoL) ('in vivo testing of novel cardioprotective compounds')



External teaching

Plymouth Microelectrode Techniques Workshop (2009 - present)


Rainbow RD, Brennan S, Jackson R, Beech AJ, Bengreed A, Waldschmidt HV, Tesmer JJ, Challiss RJ, Willets JM. (2018) Small molecule G protein-coupled receptor kinase inhibitors attenuate GRK2-mediated desensitization of vasoconstrictor-induced arterial contractions. Mol. Pharmacol. (in press)

Jackson R, Brennan S, Fielding P, Sims MW, Challiss RAJ, Adlam D, Squire IB & Rainbow RD. (2016)  Acute Vasoconstriction in Response to Elevated Glucose: Distinct Roles of PKCα and PKCβ in Mediating Inhibition of Kv Current. Brit J Pharmacol 173:870–87

Osman S, Taylor K, Allcock N, Rainbow RD & Mahut-Smith MP. (2016). Detachment of surface membrane invagination systems by cationic amphiphilic drugs. Sci Rep 6, 18536.

Panhwar F, Rainbow RD, Jackson R & Davies NW. (2015) Ca2+ dependent but PKC independent signalling mediates UTP induced contraction of rat mesenteric arteries. J Smooth Musc Res 51:58–69.

Willets JM, Nash CA, Rainbow RD, Nelson CP, & Challiss RAJ. (2015) Defining the Roles of Arrestin Isoforms in Vasoconstrictor Receptor Desensitization in Hypertension. Am J Physiol Cell 309:C179–89.

Woodier J, Rainbow RD, Stewart AJ & Pitt SJ. (2015)  Intracellular Zn2+ modulates cardiac ryanodine receptor-mediated Ca2+-release. J. Biol. Chem. 290, 17599–610.

Brennan S, Jackson R, Patel M, Sims MW, Hudman D, Norman RI, Lodwick D & Rainbow RD. (2015) Early opening of sarcolemmal ATP-sensitive K+ channels is not a key step in PKC-mediated cardioprotection. J Mol Cell Cardiol, 79:42-53

Lodwick D*, Rainbow RD*, Rubaiy HN, Al Johi M, & Norman RI. (2014)  Sulphonylurea receptors regulate the channel pore in ATP-sensitive potassium channels via an inter-subunit salt bridge. (*Joint first authors) Biochem J. 464:343–354

Sims MW, Winter J, Brennan S, Norman RI, Ng GA, Squire IB & Rainbow RD. (2014) PKC-mediated toxicity of elevated glucose concentration on cardiomyocyte function. Am J Physiol Heart, 307:H587-H597

Storey NM, Stratton RC, Rainbow RD, Standen NB, Lodwick D. (2013) Kir6.2 limits calcium overload and mitochondrial oscillations of ventricular myocytes in response to metabolic stress. Am J Physiol Heart, 305, H1508–H1518

Nelson CP, Rainbow RD, Brignell JL, Perry MD, Willets JM, Davies NW, Standen NB and Challiss RAJ. (2011)  Principal role of adenylyl cyclase in K+-channel regulation and vasodilator signalling in vascular smooth muscleCardiovasc. Res. 91:694-702

Rainbow RD, Parker AM, Davies NW. (2011) Protein kinase C-independent inhibition of arterial smooth muscle K+ channels by a diacylglycerol analogue. Br J Pharmacol. 163:845-856

Rainbow RD, Macmillan D, McCarron JG. (2009) The sarcoplasmic reticulum Ca2+ store arrangement in vascular smooth muscle. Cell CalciumNov-Dec 46 5-6 313-22

Rainbow RD, Norman RI, Everitt DE, Brignell JL, Davies NW, Standen NB.(2009) Endothelin I and angiotensin II inhibit arterial voltage-gated K+ channels through different PKC isoenzymes. Cardiovasc Res. 83 3 493-500

Currie S, Rainbow RD, Ewart MA, Kitson S, Pliego EH, Kane KA, McCarron JG.(2008) IP3R-mediated Ca2+ release is modulated by anandamide in isolated cardiac nucleiJ Mol Cell Cardiol. 6 804-11

McCarron JG, Olson ML, Rainbow RD, Macmillan D, Chalmers S.(2007) Ins(1,4,5)P3 receptor regulation during 'quantal' Ca2+ release in smooth muscle. Trends Pharmacol Sci. 2007 Jun 28 6 271-9

Chalmers S, Olson ML, MacMillan D, Rainbow RD, McCarron JG. (2007) Ion channels in smooth muscle: regulation by the sarcoplasmic reticulum and mitochondria. Cell Calcium. 42(4-5):447-466.

Rainbow RD, Hardy ME, Standen NB, Davies NW. (2006) Glucose reduces endothelin inhibition of voltage-gated potassium channels in rat arterial smooth muscle cells. J Physiol.575 Pt3 833-44

Rainbow RD, Norman RI, Hudman D, Davies NW, Standen NB. (2005) Reduced effectiveness of HMR 1098 in blocking cardiac sarcolemmal KATP channels during metabolic stress. J Mol Cell Cardiol. 39 4 637-4

Rainbow RD, Lodwick D, Hudman D, Davies NW, Norman RI & Standen NB (2004).  SUR2A C-terminal fragments reduce KATP currents and ischemic tolerance of cardiac myocytes. J Physiol,  557, 785 – 794.

Rainbow RD, James M, Hudman D, Al Johi M, Singh H, Watson PJ, Ashmole I, Davies NW, Lodwick D, & Norman RI (2004).  Proximal C-terminal domain of sulphonylurea receptor 2A interacts with the pore-forming Kir6.0 subunits in KATP channels Biochemical Journal, 379, 173 – 181.

Singh H, Hudman D, Lawrence CL, Rainbow RD, Lodwick D, & Norman RI (2003). Distribution of Kir6 and SUR2 ATP sensitive potassium channel subunits in isolated rat ventricular myocytes. J Mol cell Cardiol. 35, 445 – 459.

Lawrence CL, Rainbow RD, Davies NW, & Standen NB. (2002). Effect of metabolic inhibition on glimepiride block of native and cloned cardiac sarcolemmal KATP channels. Brit J Pharmacol, 136, 746-752.

Hudman D, Rainbow RD, Lawrence CL, & Standen, NB. (2002). The origin of calcium overload in rat cardiac myocytes following metabolic inhibition with 2,4-dinitrophenol. J Mol Cell Cardiol. 34, 859-871.

Calcium Signalling Protocols.  Third Edition


"Methods in Molecular Biology - Calcium Signalling Protocols, 3rd Edition"

Prof. D. Lambert. and Dr. Richard Rainbow (Editors)

Contributed Chapter:
"Combined Calcium Fluorescence Recording with Ionic Currents in Contractile Cells" (Rainbow, RD).


My laboratory has broad interests in cardiovascular function in health and disease. Our basic research programmes investigate the underlying mechanisms of normal cardiac and vascular function and how these are changed in disease states. Understanding these mechanistic changes in function in cardiovascular function gives us a basis for developing new therapies to treat disease states.

The research in my laboratory falls into two main research themes;

Mechanisms of cardioprotection (for addition information see here)

My laboratory started off investigating cardioprotection; a process whereby a stimulus of some kind triggers the heart to activate signalling pathways that protect the heart from damage caused by ischaemia. This stimulus can be short periods of ischaemia before a large ischaemic event (ischaemic preconditioning), short interruptions of blood flow following a major ischaemic event (post-conditioning) or by application of drug (pharmacological conditioning).

The mechanisms underlying cardioprotection are not clear, however we have identified a novel ion channel expressed at the surface of the cardiomyocyte that may play a key role in this process. This is the focus of a recently funded BHF project grant.

Further to this, the group has interests in the modulation of intracellular calcium release events. Our Leicester-based group collaborates with Dr Samantha Pitt (University of St. Andrew's) in investigating the modulation of calcium release from intracellular stores and how this differs in cardioprotection.

The effects of blood glucose and metabolism on cardiovascular function

Glucose in Blood Vessels
Glucose-induced PKC-mediated potentiation of vasoconstriction
Our initial observation was that cardioprotection afforded by most stimuli tested was abolished in the presence of high glucose. On further investigation, we have identified a common, damaging, effect of elevated blood glucose on cardiac and vascular tissue function (Sims et al (2014) and Jackson et al (2016)).

In the heart, we have shown that high blood sugar causes a change in the normal contractile function of the heart, making it more susceptible to arrhythmias. Coupled to this, glucose abolishes the natural protection that the heart can activate following severe ischaemic stress (such as angina) that can reduce the damage that occurs in a heart attack. In blood vessels glucose increases the contraction seen in response to a number of constrictor stimuli. There is a common mechanism in cardiovascular tissue where protein kinase C (PKC) appears to mediate the negative effects of glucose.

Our research techniques for investigating these two research themes range from whole tissue experimentation (wire myography for intact blood vessels and coronary ligation of the left descending coronary artery on a whole heart Langendorff perfusion system) to measuring the activity of single ion channels using patch clamp recording

Lab members

  • Dr Sean Brennan (Post-doc)
  • Abrar Alnaimi (PhD Student)
  • Simona Esposito (PhD Student)
  • Robert McKenzie (iMSc student (Sept. '18))

Former Lab members

  • Dr Alison Beech (Intercalated BSc Student)
  • Dr Shen Chen (John) (PhD Student) (Co-supervised with Dr Noel Davies)
  • Dr Shrutokirti De (Masters Student)
  • Sophie Draycott (MSc Student)
  • Dr Peter Fielding (Intercalated BSc Student and Summer 2012 Project Student)
  • Dr Robert Jackson (Intercalated BSc Student 2013 and Summer 2014 Project Student)
  • Samir Makwana (iBSc Student 2017)
  • Dr Chris Martin (F2 Medic Researcher)
  • Dr Manish Patel (Intercalated BSc Student, 2012)
  • Dr Charlotte Poile (PhD student, completed 2016)
  • Stephanie Rees (iBSc Student 2017)
  • Dr Nooraan Sheikh (Intercalated BSc Student 2014)
  • Dr Mark Sims (Intercalated BSc and Summer 2011 Project Student)

Current projects

Undergraduate project students, PhD students and Post-doctoral researchers all contribute to the ongoing research within the laboratory which currently fall into the following project areas.



I would be interested in supervising projects in the following areas:

  • Vasoconstrictor signalling in smooth muscle and the endothelium in health and disease
  • Regulation of vascular and cardiac ion channels
  • Calcium signalling in cardiomyocytes during ischaemia, reperfusion and cardioprotection
  • The role of ion channels in cardioprotection


Share this page: