Water ingestion in normal subjects increased single-unit sympathetic impulses from 42 to 58 impulses/100 beats (P<0.01) and multi-unit bursts from 36 to 51 bursts/100 beats (P<0.001).
Observational (n=9)
Absolute Event Rate: 58% vs 42%
p-value: p=<0.01
A marked pressor response to water drinking has been observed in patients with autonomic failure and in the elderly, and has been attributed to sympathetic vasoconstrictor activation, despite the absence of such a pressor response in healthy subjects with intact sympathetic mechanisms. We investigated whether water drinking in normal subjects affected peripheral sympathetic neural discharge and its effect on vascular resistance. In nine normal human subjects, we examined the effect of water ingestion on muscle sympathetic neural activity from the peroneal nerve, as multi-unit bursts (muscle sympathetic nerve activity; MSNA) and as single-unit impulses (s-MSNA) with vasoconstrictor function, and on calf vascular resistance for 120 min. In each subject, water ingestion caused increases in s-MSNA and MSNA which peaked at 30 min after ingestion; they increased respectively (mean+/-S.E.M.) from 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 vascular resistance and in plasma noradrenaline levels. A significant correlation occurred between all of these data. In conclusion, measurement of MSNA has provided direct evidence that water drinking in normal human subjects increases sympathetic nerve traffic, leading to peripheral vasoconstriction. This sympathetic activation was not accompanied by significant changes in arterial blood pressure.
Scott et al. (Mon,) conducted a observational in Healthy subjects (n=9). Water ingestion vs. Baseline was evaluated on Single-unit impulses (s-MSNA) (p=<0.01). Water ingestion in normal subjects increased single-unit sympathetic impulses from 42 to 58 impulses/100 beats (P<0.01) and multi-unit bursts from 36 to 51 bursts/100 beats (P<0.001).