Cardiac vagal response to water ingestion in normal human subjects.

In healthy young subjects there is direct evidence for sympathetic vasoconstrictor activation after drinking water, but this is not accompanied by an increase in arterial blood pressure. A marked pressor response to water ingestion has, however, been observed in elderly subjects and in patients with autonomic failure. We examined the effect of water ingestion on haemodynamic variables and heart rate variability (HRV) markers of cardiac vagal control in ten healthy young subjects and four cardiac transplant recipients with confirmed persistent cardiac vagal denervation. In a random order crossover protocol, changes in heart rate, blood pressure and measures of high frequency (HF) HRV were compared over time following the ingestion of 500 ml and 20 ml (control) of tap water. In healthy subjects, after drinking 500 ml of water the heart rate fell from 67.6+/-2.0 (mean+/-S.E.M.) to 60.7+/-2.4 beats/min (P<0.01), and the bradycardic response peaked between 20 and 25 min. There were no significant changes in arterial blood pressure. Over the same time course, water ingestion caused increases in measurements of HF HRV: root-mean-square of successive RR interval differences (RMSSD) increased by 13+/-2.7 ms after 500 ml versus 2+/-3.1 ms after 20 ml (P<0.05); HF power increased by 686+/-400 versus -63+/-322 (P<0.01). In transplant recipients water ingestion was followed by a pressor response (range 13 to 29 mmHg). These results provide evidence that water ingestion in normal subjects is followed by an increase in cardiac vagal control that may counteract the pressor effects of sympathetic activation. We suggest that in the elderly, in transplant recipients and in autonomic failure, loss of this buffering mechanism explains the pressor response to drinking water.

RCT Entities:   Population Interventions Outcomes