Dr Rich Rainbow

Research Fellow
B.Sc. (Medical Biochemistry), 1999, University Of Leicester
Ph.D. (Electrophysiology), 2003, University Of Leicester
Tel: 0116 252 3185
Email: rdr8@le.ac.uk
Address: Department of Cardiovascular Sciences, University of Leicester, Robert Kilpatrick Clinical Sciences Building, Leicester Royal Infirmary, Leicester, LE2 7LX
For general enquiries, please email the secretary, Carole Patrick, or telephone 0116 252 3183
Lab Members
Charlotte Poile (PhD Student) (Co-supervised with Prof. Iain Squire)
Manish Patel (Intercalated BSc Student) (Co-supervised with Prof. Iain Squire)
Peter Fielding (Intercalated BSc Student) (Co-supervised with Dr. Noel Davies)
Former Lab Members
Mark Sims (Intercalated BSc and Summer 2011 Project Student) (Co-supervised with Prof. Iain Squire)
Shrutokirti De (Masters Student) (Co-supervised with Dr. Dave Lodwick)
Research Interests
Blood glucose concentration is normally tightly controlled by the opposing actions of the hormones insulin and glucagon. A failure of this blood sugar regulation is termed Diabetes and can be categorised as Type-I (a loss of the ability to make insulin) or Type-II (a loss of cellular responses, or desensitisation, to insulin).
Recently Prof. Iain Squire, based within the Department of Cardiovascular Science, reported that elevations of blood glucose coincided with a higher probability of death after a myocardial infarction. Furthermore he identified that the worsened prognosis was determined not by the diabetes itself, but the high glucose concentration in the blood. These findings corroborated data gathered within my laboratory suggesting that elevated glucose could disrupt normal vascular function causing a vasoconstriction to elevate blood pressure.
Furthermore, data in cardiac ventricular cells showed that increasing extracellular glucose prolonged the duration of the cardiac action potential, depolarised the cells and increased the number of spontaneous contractions in cells; all of which are potentially pro-arrhythmic, perhaps providing a cellular mechanism for Iain’s clinical findings.
My research is primarily focussed on the effects of glucose on the cardiac ventricular and vascular smooth muscle myocyte function with particular focus on the contractile and electrophysiological function of these cells. A range of techniques are used to measure both ion channel function (patch clamp electrophysiology, wire and pressure myography, calcium imaging and cell contraction measurements) and expression (western blotting, immunohistochemistry and confocal imaging). We have also developed techniques for transfecting and virally infecting primary cardiac and smooth muscle cells to modulate channel expression/function.
Current Projects
- The effects of acute and longer-term hyperglycaemia on cardiac myocyte function (in collaboration with Prof. Iain Squire)
- The effects of acute and longer-term hyperglycaemia on ischaemic preconditioning (in collaboration with Prof. Iain Squire)
- Modulation of coronary artery tone during hyperglycaemia (in collaboration with Prof. Iain Squire and Dr. Noel Davies)
- Regulation of vascular potassium channels by protein kinases (in collaboration with Dr. Noel Davies, Dr. Jon Willets and Prof. John Challiss)
- Structure, function and regulatioin of ATP-sensitive potassium channels in vascular and cardiac tissue (in collaboration with Dr. Bob Norman and Dr. Dave Lodwick).
Membership of Learned Societies
The Physiological Society of the UK, 2001 – present
The Biophysical Society, 2001 – present
External Teaching
Plymouth Microelectrode Techniques Workshop (2009 - present)
Key Publications
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 muscle. Cardiovasc. Res. 91:694-702
Rainbow RD, MacMillan D and McCarron JG. (2009) The sarcoplasmic reticulum store Ca2+ arrangement in vascular smooth muscle. Cell Calcium 46(5-6): 313-22
Rainbow RD, Norman RI, Everitt DE, Brignell JL, Davies NW and Standen NB. (2009) Endothelin I and angiotensin II inhibit arterial voltage-gated K+ channels through different PKC isoenzymes. Cardiovasc Res. Aug 1; 83(3):493-500.
Rainbow RD, Hardy MEL, Standen NB and Davies NW. (2006). Glucose reduces endothelin inhibition of voltage-gated potassium channels in rat arterial smooth muscle cells. Journal of Physiology 575, 833–844
Rainbow RD, Lodwick D, Hudman D, Davies NW, Norman RI and Standen NB. (2004). SUR2A C-terminal fragments reduce KATP currents and ischemic tolerance of cardiac myocytes. Journal of Physiology, 557, 785–794.
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