Water ingestion increases sympathetic vasoconstrictor discharge in normal human subjects

A marked presser response to water drinking has been observed in patients w ith autonomic failure and in the elderly, and has been attributed to sympat hetic vasoconstrictor activation, despite the absence of such a presser res ponse in healthy subjects with intact sympathetic mechanisms. We investigat ed whether water drinking in normal subjects affected peripheral sympatheti c neural discharge and its effect on vascular resistance. In nine normal hu man subjects, we examined the effect of water ingestion on muscle sympathet ic neural activity from the peroneal nerve, as multi-unit bursts (muscle sy mpathetic nerve activity; MSNA) and as single-unit impulses (s-MSNA) with v asoconstrictor function, and on calf vascular resistance for 120 min. In ea ch subject, water ingestion caused increases in s-MSNA and MSNA which peake d at 30 min after ingestion; they increased respectively (mean+/-S.E.M.) fr om 42+/-4 to 58+/-5 impulses/100 beats (P < 0.01) and from 36+/-4 to 51+/-5 bursts/100 beats (P < 0.001). There were corresponding increases in calf v ascular resistance and in plasma noradrenaline levels. A significant correl ation occurred between all of these data. In conclusion, measurement of MSN A has provided direct evidence that water drinking in normal human subjects increases sympathetic nerve traffic, leading to peripheral vasoconstrictio n. This sympathetic activation was not accompanied by significant changes i n arterial blood pressure.