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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    • "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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    ABSTRACT: Frequency analysis of the electrocardiographic RR interval is a common method of quantifying autonomic outflow by measuring the beat-to-beat modulation of the heart (heart rate variability; HRV). This review identifies a series of problems with the methods of doing so-the interpretation of low-frequency spectral power, the multiple use of equivalent normalized low frequency (LFnu), high frequency (HFnu) and ratio (LF/HF) terms, and the lack of control over extraneous variables, and reviews research in the calendar year 2012 to determine their prevalence and severity. Results support the mathematical equivalency of ratio units across studies, a reliance on those variables to explain autonomic outflow, and insufficient control of critical experimental variables. Research measurement of HRV has a substantial need for general methodological improvement.
    Frontiers in Physiology 05/2014; 5:177. DOI:10.3389/fphys.2014.00177 · 3.53 Impact Factor
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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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    ABSTRACT: It has been shown that water intake (WI) improves post-exercise parasympathetic recovery after moderate-intensity exercise session. However, the potential cardiovascular benefit promoted by WI has not been investigated after high-intensity exercise. To assess the effects of WI on post-high-intensity parasympathetic recovery. Twelve recreationally active young men participated in the study (22 ± 1.4 years, 24.1 ± 1.6 kg.m-2). The experimental protocol consisted of two visits to the laboratory. Each visit consisted in the completion of a 30-min high-intensity [~80% of maximal heart rate (HR)] cycle ergometer aerobic session performing randomly the WI or control (CON, no water consumption) intervention at the end of the exercise. RR intervals (RRi) were continuously recorded by a heart rate monitor before, during and after the exercise. Differences in HR recovery [e.g., absolute heart rate decrement after 1 min of recovery (HRR60s) and time-constant of the first order exponential fitting curve of the HRR (HRRτ)] and in post-exercise vagal-related HRV indexes (rMSSD30s, rMSSD, pNN50, SD1 and HF) were calculated and compared for WI and CON. A similar HR recovery and an increased post-exercise HRV [SD1 = 9.4 ± 5.9 vs. 6.0 ± 3.9 ms, HF(ln) = 3.6 ± 1.4 vs. 2.4 ± 1.3 ms2, for WI and CON, respectively; p < 0.05] was observed in WI compared to CON. The results suggest that WI accelerates the post-exercise parasympathetic reactivation after high-intensity exercise. Such outcome reveals an important cardioprotective effect of WI.
    International journal of sport nutrition and exercise metabolism 03/2014; DOI:10.1123/ijsnem.2013-0122 · 2.44 Impact Factor
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    • "The afferent stimulus may then activate efferent sympathetic nerves at the spinal level [8]. The increase in sympathetic tone raises blood pressure in animals and in human subjects with impaired baroreflex function, the so called osmopressor response [5], [24]. We believe our study has scientific and clinical implications. "
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    ABSTRACT: Water drinking acutely increases sympathetic activity in human subjects. In animals, the response appears to be mediated through transient receptor potential channel TRPV4 activation on osmosensitive hepatic spinal afferents, described as osmopressor response. We hypothesized that hepatic denervation attenuates water drinking-induced sympathetic activation. We studied 20 liver transplant recipients (44±2.6 years, 1.2±0.1 years post transplant) as model of hepatic denervation and 20 kidney transplant recipients (43±2.6 years, 0.8±0.1 years post transplant) as immunosuppressive drug matched control group. Before and after 500 ml water ingestion, we obtained venous blood samples for catecholamine analysis. We also monitored brachial and finger blood pressure, ECG, and thoracic bioimpedance. Plasma norepinephrine concentration had changed by 0.01±0.07 nmol/l in liver and by 0.21±0.07 nmol/l in kidney transplant recipients (p<0.05 between groups) after 30–40 minutes of water drinking. While blood pressure and systemic vascular resistance increased in both groups, the responses tended to be attenuated in liver transplant recipients. Our findings support the idea that osmosensitive hepatic afferents are involved in water drinking-induced sympathetic activation in human subjects. Trial Registration NCT01237431
    PLoS ONE 10/2011; 6(10):e25898. DOI:10.1371/journal.pone.0025898 · 3.23 Impact Factor
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