The influence of chronic and acute sodium loading on blood pressure regulation in healthy normotensive adults
Date
2016
Authors
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Publisher
University of Delaware
Abstract
Excess dietary sodium intake increases cardiovascular disease risk in healthy normotensive adults independent of resting blood pressure (BP). Data using animal models suggest that high sodium (HS) in the diet alters BP regulation through serum sodium (SNa+) sensing mechanisms in the brain, leading to increased BP variability and exaggerated exercise pressor reflex activation. Acute increases in SNa+ in humans have been shown to increase resting BP and sympathetic nerve activity. No studies have addressed the time course (chronic vs. acute) effect of elevated SNa+ on BP variability and BP responses during exercise in humans. PURPOSE: To determine whether chronic and/or acute increases in SNa + lead to greater BP variability and exaggerated BP responses during exercise pressor reflex activation. HYPOTHESIS: Chronic increases in SNa+ (i.e., 7 days), but not acute increases in SNa + (23 minute hypertonic saline infusion), would increase BP variability and augment BP responses during exercise pressor reflex activation. METHODS: Chronic high SNa+ was accomplished by having normotensive participants complete 7 days of low sodium (LS; 20 mmol Na +/day) and 7 days of HS (300 mmol Na+/day) in random order, and 24h BP variability and BP responses to exercise pressor reflex activation (40% handgrip exercise followed by post exercise ischemia) were assessed on the last day of each diet. Acute high SNa+ was accomplished using a 23 minute infusion of 3% hypertonic saline; a time control (TC) trial was also performed. Four and a half minutes of BP variability was assessed prior to and following the acute infusion, as was BP and muscle sympathetic nerve responses to exercise pressor reflex activation. RESULTS: Chronic increases in sodium consumption increased 24h BP variability in only those that had an increase in SNa+ >2 mmol/L (n=24; LS: 10.9±0.5, HS= 12.9±0.6 mmHg, p<0.05). Acute increases in SNa+ had no effect on BP variability (n=18; 4.4±0.5 vs. 4.3±0.4 mmHg, p>0.05). In response to exercise pressor reflex activation, chronic increases in SNa+ increased systolic BP responses during exercise pressor reflex activation (n=16; LS=137.2±4.1 mmHg vs. HS=145.9±4.1 mmHg, p<0.05). While acute increases in SNa+ raised sympathetic outflow (pre=11±2 vs. post=15±2 bursts/min, p<0.05) but had no effect on BP responses to exercise pressor reflex activation (p>0.05). CONCLUSION: Chronic increases in SNa+ increase 24h BP variability and systolic BP responses to exercise pressor reflex response activation, while acute increases in SNa+ have no effect on short-term (4.5 minutes) BP variability or BP responses during exercise pressor reflex activation. These data provide evidence that alterations in SNa + influence BP regulation in normotensive adults.