The osmopressor response to water drinking

Institute of Clinical Pharmacology, Hannover, Germany.
AJP Regulatory Integrative and Comparative Physiology (Impact Factor: 3.11). 11/2010; 300(1):R40-6. DOI: 10.1152/ajpregu.00544.2010
Source: PubMed


Water drinking elicits profound pressor responses in patients with impaired baroreflex function and in sinoaortic-denervated mice. Healthy subjects show more subtle changes in heart rate and blood pressure with water drinking. The water-induced pressor response appears to be mediated through sympathetic nervous system activation at the spinal level. Indeed, water drinking raises resting energy expenditure in normal weight and obese subjects. The stimulus setting off the response is hypoosmolarity rather than water temperature or gastrointestinal stretch. Studies in mice suggest that this osmopressor response may involve transient receptor potential vanniloid 4 (Trpv4) receptors. However, the (nerve) cell population serving as peripheral osmosensors and the exact transduction mechanisms are still unknown. The osmopressor response can be exploited in the treatment of orthostatic and postprandial hypotension in patients with severe autonomic failure. Furthermore, the osmopressor response acutely improves orthostatic tolerance in healthy subjects and in patients with neurally mediated syncope. The phenomenon should be recognized as an important confounder in cardiovascular and metabolic studies.

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Available from: Marcus May, Nov 17, 2015
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    • "Of these, the most attention has been paid to water consumption (May and Jordan, 2011) subsequent to the finding that patients with severe hypotension due to autonomic failure derived a significant reduction in symptoms from drinking water, and this subjective improvement was observed parallel to substantial increases in blood pressure (Jordan et al., 2000). A similar effect can be observed when the baroreflex loop is opened in sinoaortically denervated mice (McHugh et al., 2010). "
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    • "One of the hypothesis lies on the presence of mechanoreceptors in stomach that when stimulated by gastric distention, causes a reflex increase in sympathetic efferent activity (Rossi et al. 1998; van Orshoven et al. 2004). Some recent investigations have also linked this sympathetic response to the activation of TRPV4 osmolarity-sensitive receptors within the portal and intestinal circulation (May & Jordan, 2011; McHugh et al., 2010). In order to avoid an acute blood pressure increase, Routledge et al. (2002) and Brown et al. (2005) have shown that this vasoconstrictive sympathetic response is immediately counterbalanced by a concomitant increase in cardiac vagal activity which promotes a bradycardic effect. "
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