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 RegistrationClinicalTrials.gov NCT01237431
Highlights
Water drinking acutely increases sympathetic activity in human subjects [1,2,3,4]
The main finding of our study is that in liver transplant recipients plasma norepinephrine increases after water drinking less as compared to the response in kidney transplant recipients
The observation may suggest that hepatic afferent nerves are involved in the sympathetic activation associated with water drinking
Summary
Water drinking acutely increases sympathetic activity in human subjects [1,2,3,4]. The response elicits a profound increase in blood pressure in patients with impaired baroreflex function [1]. Water ingestion raises blood pressure in sinoaortic denervated but not in baroreflex intact mice [5]. We identified hepatic spinal afferents in mice detecting physiological shifts in blood osmolality through activation of the transient receptor potential vanilloid cation channel 4 (TRPV4) [10]. Genetic TRPV4 deletion, abolishes the water drinking-induced pressor response [5]. We hypothesized that hepatic afferent nerves are involved in the sympathetic activation associated with water drinking and that hepatic denervation attenuates the response.
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