I began working on salt and water homeostasis as a medical student in 1991. At that time, the generally accepted belief was that body Na+ content is constant, and that any increase would elevate blood pressure. Measuring Na+ balance in humans preparing for long-term space missions, however, we found that rhythmically Na+ dis- and re-appeared from an at that time invisible storage site. Developing novel tools, we saw that rodents and humans store large amounts of Na+ under their skin and in skeletal muscle, and that the storage process is physiologically regulated. This new way of thinking about the body fluids quickly delivered new research avenues in immunology (immunological host defence and auto-immunity), endocrinology (insulin resistance, diabetes mellitus, and metabolic muscle function), and cardiovascular disease (hypertension research, heart failure). Today, our clinical research revolves around the fact that Na+ storage is secondary to intracellular K+ depletion, and that increasing K+ intake effectively reverses this process; with beneficial effects on blood pressure. In the basic research arena, we dream of solving a general methodological-physiological root problem in the field: our inability to visualize and quantify Na+ and K+ distribution disorders inside diseased cells at the µm scale in intact, hydrated organs.

Alta (Aletta E.) Schutte PhD FESC FRRSAf ISHF is SHARP Professor and Principal Theme Lead of Cardiac, Vascular and Metabolic Medicine in the Faculty of Medicine and Health at UNSW Sydney, Australia. She is also the Global Co-Director of the Cardiovascular Program and Head of the Blood Pressure Program at The George Institute for Global Health. She is a NHMRC Investigator Grant Leadership Fellow. She has extensive experience in working in clinical and population-based studies with a focus on raised blood pressure, hypertension and cardiovascular disease. She has been the Chief Investigator of several multidisciplinary studies, published >500 papers in the field of blood pressure and cardiovascular disease, and supervised over 85 postgraduate students. She is the senior author of the 2020 International Society of Hypertension Global Hypertension Guidelines. She has been acknowledged for her work as winner of several awards, most recently the 2022 Harriet Dustan Award of the American Heart Association's Hypertension Council and 2023 Peter Sleight Excellence Award in Hypertension Clinical Research from the World Hypertension League. In 2023 and again in 2024, she was recognised as the Leading Researcher in Vascular Medicine by The Australian, and in 2024 received the Fiona Stanley Award from the NHMRC as the highest ranked applicant awarded with a $5 million SYNERGY grant. She serves as Associate Editor of Hypertension and is on the Editorial Board of several major hypertension and cardiovascular journals. She is Company Secretary of the Australian Cardiovascular Alliance, Board Member of Hypertension Australia, Fellow of the European Society of Cardiology, the International Society of Hypertension and the Royal Society of South Africa, and Past President of the International Society of Hypertension (ISH). She is Co-Chair of the National Hypertension Taskforce of Australia.

Professor Andrew Murphy obtained a BSc(Hons) in Biotechnology from the Queensland University of Technology (QUT) in Brisbane and a PhD (Monash University) at the Baker Heart and Diabetes Institute, funded by an industry scholarship from the Swiss biotech company Actelion. During this time, he discovered an anti-inflammatory role for HDL on circulating monocytes and neutrophils both published in ATVB. Upon completing his PhD, Andrew moved to Columbia University in New York under Professor Alan Tall, where he was funded by a prestigious American Heart Association Fellowship. His work shifted to examining the role of cholesterol efflux pathways on the proliferation and mobilisation of haematopoietic stem cells (HSCs) in the bone marrow. Specifically, he defined a cell-intrinsic role for ApoE in regulating HSC proliferation and showed that increased numbers of circulating monocytes resulted in larger lesions, which was published in the Journal of Clinical Investigation. He also discovered the haematopoietic role of the cholesterol transporter ABCG4 in platelet production and atherosclerosis, along with defining an important feedback loop for the thrombopoietin receptor c-MPL, published in Nature Medicine. Professor Murphy also initiated several collaborations in New York, in particular with Professor Ira Goldberg and Professor Edward Fisher (NYU) along with A/Professor Prabhakara Nagareddy (University of Oklahoma Health and Sciences Center) to explore the mechanisms of diabetes (hyperglycaemia) on monocyte production. They were the first to show that the novel glucose-lowering agent (SGLT2 inhibitors) could reduce circulating monocyte levels and facilitate atherosclerotic lesion regression. They discovered the damage associated molecular pattern molecules as important mediators of this event. These studies published in Cell Metabolism have triggered an extensive and collaborative research program run by these investigators with publications in Cell Metabolism, Circulation and Circulation Research, Journal of Clinical Investigation, etc.