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.

Michael is currently Director of the Hypertension Units and of the Endocrine Hypertension Research Centre within the University of Queensland Frazer Institute at Greenslopes and Princess Alexandra Hospitals in Brisbane. He has over 30 years clinical research experience in pathogenesis and management of hypertension and especially of endocrine varieties including primary aldosteronism, renovascular hypertension, pheochromocytoma and familial hyperkalemic hypertension. Working with mentor Richard Gordon, he helped to demonstrate that primary aldosteronism is at least 10 times more common than previously thought, and is the commonest specifically treatable and potentially curable form of hypertension. Subsequent studies have involved determining genetic bases for primary aldosteronism, examining non-blood pressure dependent effects of aldosterone excess, improving methods of detection, diagnostic workup and management of primary aldosteronism, exploring the pathogenesis and genetics of other salt sensitive forms of hypertension (including familial hyperkalemic hypertension) and investigating how dietary potassium lowers blood pressure.