Salt Loading Affects Cortisol Metabolism in Normotensive Subjects: Relationships with Salt Sensitivity

Kerstens, Michiel N.; Kleij, Frank G.H. van der; Boonstra, A. H.; Sluiter, Wim J.; Koerts, Jasper; Navis, Gerjan; Dullaart, Robin P. F.

doi:10.1210/jc.2002-021625

Cited by 33 publications

(23 citation statements)

References 28 publications

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“…We show that the projected combined effect of salt- rone excretion, but also increased cortisol and cortisone excretion in the urine (11). This finding is in line with the study by Kerstens et al that examined the effect of dietary salt ingestion on glucocorticoid excretion in salt-resistant subjects under daily life conditions (34). Thus, a 6-g/d increase in salt intake induces a catabolic hormone profile in humans.…”

Section: Hypothesis 2: Dietary Salt Modulates Endogenous Infradianrhysupporting

confidence: 92%

Increased salt consumption induces body water conservation and decreases fluid intake

Rakova¹,

Kitada²,

Lerchl³

et al. 2017

Journal of Clinical Investigation

131

122

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BACKGROUND. The idea that increasing salt intake increases drinking and urine volume is widely accepted. We tested the hypothesis that an increase in salt intake of 6 g/d would change fluid balance in men living under ultra-long-term controlled conditions. METHODS.Over the course of 2 separate space flight simulation studies of 105 and 205 days' duration, we exposed 10 healthy men to 3 salt intake levels (12, 9, or 6 g/d). All other nutrients were maintained constant. We studied the effect of salt-driven changes in mineralocorticoid and glucocorticoid urinary excretion on day-to-day osmolyte and water balance. RESULTS.A 6-g/d increase in salt intake increased urine osmolyte excretion, but reduced free-water clearance, indicating endogenous free water accrual by urine concentration. The resulting endogenous water surplus reduced fluid intake at the 12-g/d salt intake level. Across all 3 levels of salt intake, half-weekly and weekly rhythmical mineralocorticoid release promoted free water reabsorption via the renal concentration mechanism. Mineralocorticoid-coupled increases in free water reabsorption were counterbalanced by rhythmical glucocorticoid release, with excretion of endogenous osmolyte and water surplus by relative urine dilution. A 6-g/d increase in salt intake decreased the level of rhythmical mineralocorticoid release and elevated rhythmical glucocorticoid release. The projected effect of salt-driven hormone rhythm modulation corresponded well with the measured decrease in water intake and an increase in urine volume with surplus osmolyte excretion. CONCLUSION.Humans regulate osmolyte and water balance by rhythmical mineralocorticoid and glucocorticoid release, endogenous accrual of surplus body water, and precise surplus excretion.

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Section: Hypothesis 2: Dietary Salt Modulates Endogenous Infradianrhysupporting

confidence: 92%

Increased salt consumption induces body water conservation and decreases fluid intake

Rakova¹,

Kitada²,

Lerchl³

et al. 2017

Journal of Clinical Investigation

131

122

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“…Young normotensive ss subjects do not reduce their peripheral cortisol levels nor increase urinary cortisol metabolite elimination under a high-salt diet as sr subjects do, 32 in line with the prior finding that cortisol excretion decreases under low-salt conditions in healthy subjects. 33 In accordance, subjects with the highest free cortisol excretion show the least sensitivity of BP to dietary sodium loading.…”

Section: Introductionsupporting

confidence: 89%

“…[50][51][52] Our finding, however, conflicts with another study in young healthy Caucasians where no differences between 9 ss and 19 sr subjects were found in morning cortisol levels (0830) during both high-and low-salt intake, despite differences in the urinary cortisol excretion, suggesting a cortisol excess in the ss under the high-salt intake. 32 However, cortisol levels vary highly depending on daytime and other factors, restricting comparison across studies.…”

Section: Cortisolmentioning

confidence: 99%

Salt-sensitive men show reduced heart rate variability, lower norepinephrine and enhanced cortisol during mental stress

et al. 2008

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Salt sensitivity (SS) represents a risk factor for essential hypertension, which has been related to enhanced cardiovascular stress reactivity possibly mediated by increased noradrenergic susceptibility. We investigated biophysiological responses to mental stress in salt-sensitive (ss) and salt-resistant (sr) subjects, hypothesizing lower heart rate variability (HRV) and higher cortisol in the ss. A total of 48 healthy normotensive Caucasian men (age 25.6±2.6, body mass index 22.9±2.3) were phenotyped for SS (defined as significant drop in mean arterial pressure43 mm Hg under the low-salt diet) by a 2-week high-versus low-salt diet. Subjects underwent a standardized mental stress task with continuous cardiovascular monitoring before, during and after the test (Finapres; Ohmeda, Louisville, CO, USA). Blood samples were drawn to examine cortisol and catecholamines before, after and 20 min after stress. The task elicited significant increases of systolic blood pressure (SBP), diastolic BP (DBP) and heart rate (HR) and a significant decrease of HRV (all time effects Po0.0001). The ss subjects showed lower norepinephrine (NE) and higher cortisol, indicated by significant group effects (P ¼ 0.009 and 0.025, respectively). HR increased and HRV decreased more in the ss under the stress, shown by significant time by group interactions (P ¼ 0.045 and 0.003, respectively). The observation of a more pronounced HR rise coupled with a greater decrease of HRV in healthy ss men under the influence of brief mental stress confirms their enhanced physiological stress reactivity. The lower peripheral NE may represent an effort to compensate for increased noradrenergic receptor sensitivity. The enhanced cortisol levels are backed by recent genetic findings on HSD11B2 polymorphisms and may promote hypertension.

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“…We have adjusted for these confounders in the regression analyses. Kerstens et al [7] did not comment on confounding by these or other factors.…”

mentioning

confidence: 97%

“…Kerstens et al [7] studied cortisol metabolism, insulin sensitivity (according to homeostasis model assessment of insulin resistance [HOMA-IR]) and renal haemodynamics in 19 salt-resistant and nine salt-sensitive normotensive subjects after a low-and high-salt diet. Although in their letter [1] Kerstens and Dullaart pass comment on their observation of a significant positive relationship between percentage change in HOMA-IR and percentage change in plasma cortisol during salt loading [7] (at variance with our findings), it should be noted that in the same study [7] they also describe a significant inverse relationship between percentage change in HOMA-IR and percentage change in the sum of urinary metabolites (in keeping with our findings). Moreover, the authors studied young men and women (mean age 24 years) who were lean (mean BMI 22 kg/m 2 ).…”

mentioning

confidence: 99%

Insulin resistance and cortisol metabolism. Reply to Kerstens MN, Dullaart RPF [letter]

2007

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Abbreviations HOMA-IR homeostasis model assessment of insulin resistanceTo the Editor: We thank M. N. Kerstens and R. P. F. Dullaart for their interest in our paper [1]. Our results show that there was an inverse relationship between cortisol clearance from the plasma and whole-body insulin sensitivity as measured by the hyperinsulinaemic-euglycaemic clamp in middle-aged men (mean age 53.0 years, mean. Importantly, we show that this relationship was independent of potential confounding factors such as body fat and fatty liver. These findings were contrary to our expectations and we agree that it is now crucial to undertake careful kinetic studies to study cortisol production (and excretion) in more detail to determine specifically whether cortisol production is increased. We agree that by measuring urinary free cortisol we have only assessed a small fraction of all urinary cortisol metabolites. It is possible that there is increased renal loss of cortisol with insulin resistance that we have not detected. We appreciate that we have not assessed salt resistance in our subjects, but there is no consensus as to whether salt loading worsens, improves, or has no effect on insulin sensitivity [3][4][5][6]. Kerstens et al. [7] studied cortisol metabolism, insulin sensitivity (according to homeostasis model assessment of insulin resistance [HOMA-IR]) and renal haemodynamics in 19 salt-resistant and nine salt-sensitive normotensive subjects after a low-and high-salt diet. Although in their letter [1] Kerstens and Dullaart pass comment on their observation of a significant positive relationship between percentage change in HOMA-IR and percentage change in plasma cortisol during salt loading [7] (at variance with our findings), it should be noted that in the same study [7] they also describe a significant inverse relationship between percentage change in HOMA-IR and percentage change in the sum of urinary metabolites (in keeping with our findings). Moreover, the authors studied young men and women (mean age 24 years) who were lean (mean BMI 22 kg/m 2 ). In contrast, we studied middle-aged men only and our volunteers were predominantly obese. The relationships between cortisol metabolism and insulin sensitivity may differ in insulin-resistant, obese individuals Diabetologia

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Salt Loading Affects Cortisol Metabolism in Normotensive Subjects: Relationships with Salt Sensitivity

Cited by 33 publications

References 28 publications

Increased salt consumption induces body water conservation and decreases fluid intake

Increased salt consumption induces body water conservation and decreases fluid intake

Salt-sensitive men show reduced heart rate variability, lower norepinephrine and enhanced cortisol during mental stress

Insulin resistance and cortisol metabolism. Reply to Kerstens MN, Dullaart RPF [letter]

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