We are grateful to Simon Thornton for his Correspondence (Salt intake, cardiovascular disease, and physiology. Nat. Rev. Cardiol. https://doi.org/10.1038/s41569-018-0047-3; 2018)1 on our Review (Role of salt intake in prevention of cardiovascular disease: controversies and challenges. Nat. Rev. Cardiol. 15, 371–377; 2018)2. However, our Review was focused on the evidence that salt intake is a major determinant of population blood pressure, not on the mechanisms by which salt can cause high blood pressure.

We and others have published several papers on the potential mechanisms3,4,5 but we did not think that this information was directly relevant to public health. When humans consume more salt, plasma levels of sodium and chloride increase, which causes increased thirst and fluid consumption. At the same time, this increase in the sodium and chloride concentrations increases extracellular fluid volume. Under normal circumstances, this increase in extracellular volume suppresses the renin–angiotensin–aldosterone system and also increases release of atrial natriuretic peptide (ANP), which to some extent mitigates the rise in blood pressure that would have occurred. However, long-term small increases in extracellular — or, more accurately, intrathoracic — volume slowly raise blood pressure.

In studies that we and others have performed, when individuals increase their water intake, transient increases in body weight can occur but these are very short-term6. In studies with healthy volunteers, increasing fluid intake from around 1 l to 6 l per day resulted in no changes in body weight, blood pressure, or aldosterone and ANP levels, but large changes occurred in levels of antidiuretic hormone, as one would expect6. These and other studies clearly show that water does not, in itself, have any effect on extracellular volume, but has a purely passive role when thirst is increased by an increase in sodium or chloride concentration.