We’ve known for a long time that the Na/K pump is important in the control of blood pressure. However, this study identifies a novel mechanism that could be targeted to provide a new therapeutic approach to treating ageing-induced hypertension
Mike Shattock, Professor of Cellular Cardiology.
06 January 2021
Researchers identify a possible new target for treatment of hypertension
New study examines how changes in protein in arterial smooth muscle cells affect blood pressure and hypertension.
Researchers, led by Professor Mike Shattock, from the School of Cardiovascular Sciences, have recently published a study suggesting that changes in a protein regulating the transport of sodium in arterial smooth muscle cells can significantly affect blood pressure, and contribute to hypertension.
Arterial smooth muscle maintains a low intracellular concentration of sodium by pumping out Na of the cell via a protein called the Na/K pump. This research, funded by the British Heart Foundation, and involving a collaboration between the team at King’s and colleagues at the University of Glasgow, University of Oxford, Dundee University, and Queen Mary University of London, highlights the role of a key regulator of the Na/K pump: phospholemman.
The study demonstrates that changes in the phosphorylation of phospholemman profoundly influence both the vascular tone and blood pressure in mice, and that these changes correlate with essential hypertension in old age.
By searching through human genomic databases, the team discovered a rare mutation in phospholemman that actually prevents its phosphorylation; this is associated with a significantly elevated blood pressure in middle-aged men.
In recent years we have developed a really detailed understanding of how the protein phospholemman controls essential processes in the heart. This new study has drawn in unique expertise from our colleagues around the UK to uncover a completely new role for phospholemman in blood pressure control. We’re particularly excited because our findings could open the door to completely new treatments for a condition that is notoriously difficult to treat
Dr William Fuller (co-author, University of Glasgow).
Read their full paper, published in the journal Circulation.
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Professor of Cellular Cardiology