Dr Peter Flatman

Personal profile

• 1980 - present: Lecturer, then Senior Lecturer, The University of Edinburgh
• 1977 - 1980: MRC Research Assistant, Cambridge University
• 1974 - 1975: Michael Foster Student, Cambridge University
• 1974 - 1977: MRC Research Student, Cambridge University
• MA PhD Cambridge University

Research

Dr Peter Flatman's research briefing

My work has focused on the roles of magnesium and protein phosphorylation in regulating transport by the sodium pump, and by members of the cation-chloride-cotransporter family (Slc12A), including NKCC1, NKCC2 (Na-K-2Cl cotransporters), KCC (K-Cl cotransporter) and NCC (Na-Cl cotransporter). I have also worked on cell magnesium homeostasis, quantifying the roles of cytoplasmic buffers, and of transport through channels and a sodium-magnesium antiport.

These processes play key roles in regulating cell volume and composition, and in epithelial reabsorption and secretion. Their dysfunction results in several prevalent diseases, and I am currently working on their role in causing and maintaining high blood pressure.

The stress hormones, glucocorticoids (e.g. cortisol in humans), are known to increase blood pressure but their mechanism of action is unclear. Hypertension caused in this way is an important clinical problem and requires better, targeted treatment. We are exploring how these hormones affect the reabsorption of sodium in the kidney by the Na-Cl cotransporter (NCC). We are examining how modifications to NCC, particularly its phosphorylation at several sites, affects sodium transport and thiazide response, and aim to establish the extent to which changes in NCC activity cause and/or maintain this type of hypertension.

Collaborations

• Dr M A Bailey (QMRI, University of Edinburgh)

Selected Publications

Ivy J. R., Oosthuyzen W., Peltz T. S., Howarth A. R., Hunter R. W., Dhaun N., Al-Dujaili E. A. S., Webb D. J., Dear J. W., Flatman P. W. & Bailey M. A. (2016). Glucocorticoids Induce Nondipping Blood Pressure by Activating the Thiazide-Sensitive Cotransporter. Hypertension 67, 1029-1037.

Heye A. K., Thrippleton M. J., Chappell F. M., Valdés Hernández M. dC., Armitage P. A., Makin S. D., Muñoz Maniega S., Sakka E., Flatman P. W., Dennis M. S. & Wardlaw J. M. (2016). Blood pressure and sodium: Association with MRI markers in cerebral small vessel disease. Journal of Cerebral Blood Flow and Metabolism 36, 264-274.

Hunter RW, Ivy JR, Flatman PW, Kenyon CJ, Craigie E, Mullins LJ, Bailey MA & Mullins JJ. (2015). Hypertrophy in the Distal Convoluted Tubule of an 11β-Hydroxysteroid Dehydrogenase Type 2 Knockout Model. Journal of the American Society of Nephrology 26, 1537-1548.

Ashek, A., Menzies, R. I., Mullins, L. J., Bellamy, C. O. C., Harmar, A. J., Kenyon, C. J., Flatman, P. W., Mullins, J. J., & Bailey, M. A. (2012). Activation of Thiazide-Sensitive Co-Transport by Angiotensin II in the cyp1a1-Ren2 Hypertensive Rat. PLoS ONE 7, e36311.

Hannemann A & Flatman PW (2011). Phosphorylation and Transport in the Na-K-2Cl Cotransporters, NKCC1 and NKCC2A, Compared in HEK-293 Cells. PLoS ONE 6, e17992.

Hannemann A, Christie JK & Flatman PW (2009). Functional Expression of the Na-K-2Cl Cotransporter NKCC2 in Mammalian Cells Fails to Confirm the Dominant-negative Effect of the AF Splice Variant. Journal of Biological Chemistry 284, 35348-35358.

Flatman PW (2008) Cotransporters, WNKs and hypertension: an update. Current Opinion in Nephrology and Hypertension 17:186-192.

Flatman PW (2007) Cotransporters, WNKs and hypertension: important leads from the study of monogenetic disorders of blood pressure regulation. Clinical Science 112: 203-216.

Almulla HA, Bush PG, Steele MG, Flatman PW, Ellis, D (2006) Sodium-dependent recovery of ionised magnesium concentration following magnesium load in rat heart myocytes. Pflügers Archiv - European Journal of Physiology 451: 657-667.

Peter Flatman publication list (PDF)