Water drinking is recognized to be an essential behavior for fluid homeostasis and is frequently and necessarily observed in daily life. Water drinking causes many physiological changes, including fluctuations in endocrine function, cardiovascular system, and fluid balance during or immediately after drinking [1][2][3][4][5][6][7]. Because these changes occur in the early phase of drinking, the contribution of absorbed water from the gastrointestinal tract may be little, if any, but neural factors such as reflex, as with receptors in the oral, pharyngeal, esophageal, or gastric regions, have been suggested. Stimulation of the oropharyngeal region with water results in a decreased release of vasopressin and causes hypotonic diuresis in humans [1]. Recently, we have demonstrated that water drinking caused a biphasic change in blood volume; an initial hemoconcentration followed by hemodilution in humans [2]. The initial hemoconcentration was likely to be induced by a transient rise in blood pressure (BP) immediately after the onset of drinking. The rise in BP following water drinking by animals and humans might be attributed to stimuli from the oropharyngeal region, gastric distension, or other stimuli [3,[8][9][10], however, the mechanism responsible for the drinking- Japanese Journal of Physiology, 52, 421-427, 2002 Key words: pressor response, microneurography, water ingestion, gastric distension, human.
Abstract:To investigate the possible involvement of the sympathetic nervous system in pressor response during water drinking, muscle sympathetic nerve activity (MSNA), blood pressure (BP), and heart rate (HR) were continuously measured in healthy young volunteers throughout the experiments of a 5-min control, 2 min of drinking 500 ml water, and a 28-min recovery. To avoid the effects of water passing through the oropharyngeal and esophageal regions and/or effects of swallowing, an equal amount of water was directly infused to the stomach through a stomach tube for 2 min. Water drinking caused a transient increase in mean arterial pressure (MAP) and HR immediately after drinking (⌬MAP, 12.6Ϯ2.1 mmHg; ⌬HR, ϩ19.9Ϯ1.7 beats/min at the peak). An abrupt decrease of MSNA was observed directly during water drinking (⌬burst rate, Ϫ6.9Ϯ1.3 bursts/min; ⌬total activity, Ϫ2,606Ϯ 491 U/min), and it increased to the baseline level thereafter. Gastric infusion had little or no effect on MAP, HR, and MSNA. The present study demonstrated that a pressor response during water drinking was associated with the attenuation of MSNA and not generated by gastric infusion of water at the same rate as in this drinking manner. In conclusion, the rapid rise in BP might be caused through stimulations from the oropharyngeal region, swallowing-induced factors, and/or a feedforward mechanism by a central descending signal from the higher brain centers.