In studies of the effects of salt intake on blood pressure (SBP, MBP, DBP), influences on heart rate (HR) are usually neglected even though the longterm load on both left ventricle (LV) and systemic arteries (SA) is better related to the product of HR x SBP (or MBP) than to pressure alone. After all, altered salt intakes often induce considerable volume-related changes in HR, and the heart operates more economically at low HR and high stroke volume (SV). Thus, about 3/4 of LV metabolism is used for the build-up of systolic tension, while the cost for SV expulsion, or for SV increases, is far lower. Moreover, low HR prolongs the diastolic period, so important for LV coronary supply. Against this background we have used results from studies in both rats and man, in which both BP and HR were followed during marked changes in salt intake, to explore how this affected the HR x SBP (or HR x MBP) product. Briefly, in ordinarily salt-resistant organisms, whether normo- or hypertensive, salt intake increases, which in man ranged from 10-20 to 250-300 mM (in rats over 100-fold), if anything reduced the computed longterm load (HR x SBP, or MBP) on LV and SA, as consequences of an efficient reflex volume control. By contrast, in salt-sensitive man, HR reflex reductions to increased salt intake were almost absent despite substantial SBP elevations, suggesting the influence of a CNS suppression of bulbar reflex centres combined with CNS neurohormonal interference with renal salt volume excretion, as in SHR.