Water deprivation does not augment sympathetic or pressor responses to sciatic afferent nerve stimulation in rats or to static exercise in humans

Abstract

Excess dietary salt intake excites central sympathetic networks, which may be related to plasma hypernatremia. Plasma hypernatremia also occurs following water deprivation (WD). The purpose of this study was to test the hypothesis that WD induces hypernatremia and consequently augments sympathetic and pressor responses to sympathoexcitatory stimuli in rats and humans. Sympathetic nerve activity (SNA) and arterial blood pressure (ABP) responses to sciatic afferent nerve stimulation (2-20 Hz) and chemical stimulation of the rostral ventrolateral medulla (RVLM) were assessed in rats after 48 h of WD and compared with normally hydrated control rats (CON). In a parallel randomized-crossover human experiment (n = 13 healthy young adults), sympathetic (microneurography) and pressor (photoplethysmography) responses to static exercise were compared between 16-h WD and CON conditions. In rats, plasma [Na+] was significantly higher in WD versus CON [136 ± 2 vs. 144 ± 2 (SD) mM, P < 0.01], but sciatic afferent nerve stimulation produced similar increases in renal SNA [5 Hz, 174 ± 34 vs. 169 ± 49% (SD), n = 6-8] and mean ABP [5 Hz, 21 ± 6 vs. 18 ± 7 (SD mmHg, n = 6-8]. RVLM injection of l-glutamate also produced similar increases in SNA and ABP in WD versus CON rats. In humans, WD increased serum [Na+] [140.6 ± 2.1 vs. 142.1 ± 1.9 mM (SD), P = 0.02] but did not augment sympathetic [muscle SNA: change from baseline (Δ) 6 ± 7 vs. 5 ± 7 (SD) bursts/min, P = 0.83] or mean ABP [Δ 12 ± 5 vs. 11 ± 8 (SD) mmHg, P = 0.73; WD vs. CON for all results] responses during the final minute of exercise. These findings suggest that despite eliciting relative hypernatremia, WD does not augment sympathetic or pressor responses to sciatic afferent stimulation in rats or to static exercise in humans. NEW & NOTEWORTHY Excess dietary salt intake excites central sympathetic networks, which may be related to plasma hypernatremia. Plasma hypernatremia also occurs following water deprivation (WD). We sought to determine whether plasma hypernatremia/hyperosmolality induced by WD augments sympathetic and pressor responses to sympathoexcitatory stimuli. Our findings suggest that WD does not augment sympathetic or pressor responses to sciatic afferent nerve stimulation in rats or to static exercise in humans.

Keywords: exercise pressor reflex; hypernatremia; hypohydration; sciatic nerve stimulation; sympathetic nerve activity.

Conflict of interest statement

No conflicts of interest, financial or otherwise, are declared by the authors.

Figures

Fig. 1.

Representative tracings of arterial blood pressure (ABP), mean ABP (superimposed white lines), heart rate, and rectified/integrated and raw lumbar sympathetic nerve activity (SNA), renal SNA, and splanchnic (Spl) SNA of control (CON) and water-deprived (WD) rats during electrical stimulation of sciatic nerve afferents at 5 and 10 Hz (1-ms pulse, 5-s train). Here, bpm, beats/min.

Fig. 2.

Summary data (means ± SD) with individual data points of peak changes in mean arterial blood pressure (ABP), heart rate, lumbar sympathetic nerve activity (SNA), renal SNA, and splanchnic SNA of control and water-deprived (WD) rats during electrical stimulation of the sciatic nerve (2, 5, 10, and 20 Hz; 1-ms pulse, 5-s train). Electrical stimulation of sciatic afferent nerves increased SNA and ABP in both groups (P < 0.05 frequency factor from overall ANOVA). Post hoc tests (independent t-tests with layered Bonferroni correction) revealed a frequency-dependent increase in SNA and ABP between 2 and 5 Hz within a group (*P < 0.05). However, there were no significant differences in any variable between control and WD rats (P > 0.133–0.819 group factor of overall ANOVAs). Here, bpm, beats/min.

Fig. 3.

A: 60-s examples of arterial blood pressure (ABP), mean ABP (superimposed white lines), and rectified/integrated lumbar sympathetic nerve activity (SNA), renal SNA, and splanchnic (Spl) SNA of control and water-deprived (WD) rats during rostral ventrolateral medulla (RVLM) injection of l-glutamate. Arrowheads indicate injection. B: summary data (means ± SD) with individual data points of peak changes in mean ABP and SNA of control and WD rats after RVLM injection of l-glutamate. Glutamate produced concentration-dependent increases in SNA and ABP (P < 0.05, overall ANOVA for concentration factor, *P < 0.05 vs. lower concentration via paired t-test). However, there were no statistical differences between groups for any variable (P > 0.2 for group factor of overall ANOVAs). C: schematic illustration and digital images of injection sites for control (left side of illustration and top digital image) and WD (right side of illustration and bottom digital image).

Fig. 4.

A: 500-s examples of arterial blood pressure (ABP), mean ABP (superimposed white lines), and rectified/integrated lumbar sympathetic nerve activity (SNA), renal SNA, and splanchnic (Spl) SNA of control and water-deprived (WD) rats during rostral ventrolateral medulla (RVLM) injection of 333 mM GABA (30 nl). Arrowheads indicate injection. B: summary data (means ± SD) with individual data points of peak changes in mean ABP and SNA of control and WD rats after RVLM injection of GABA. Individual data points are superimposed. GABA produced concentration-dependent decreases in ABP and SNA (P < 0.05, overall ANOVA for concentration factor, *P < 0.05 vs. lower concentration via paired t-test). However, there were no statistical differences between groups for any variable (P > 0.3 group factor overall ANOVAs). C: schematic illustration and digital images of injection sites for control (left side of illustration and top digital image) and WD (right side of illustration and bottom digital image).

Fig. 5.

Representative beat-to-beat arterial blood pressure (ABP), muscle sympathetic nerve activity (SNA), and handgrip force tracings from one participant in both experimental conditions.

Fig. 6.

Summary data (means ± SD) with individual data points (n = 13) of absolute mean arterial blood pressure (ABP; A), mean ABP absolute change from baseline (BASE; B), absolute muscle sympathetic nerve activity (SNA; C), and muscle SNA absolute change from baseline (D; expressed as burst frequency for both C and D) during 2 min of handgrip exercise (HG) and 3 min of postexercise ischemia (PEI). Two-way repeated-measures ANOVA (time × condition), *P < 0.05 for a time effect. CON, control condition; WD, water deprivation condition.