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Interaction of Stress and Dietary NaCl Intake in Hypertension: Renal Neural Mechanisms

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Abstract

A synthesizing concept of the development of primary hypertension is that it arises from an interaction of genetic and environmental factors. Of the environmental factors, dietary NaCl intake and mental stress are among the most thoroughly investigated. This review will focus on the interaction between genetic predisposition and the environmental influences of dietary NaCl intake and mental stress in the development of primary hypertension. © 2013 American Physiological Society. Compr Physiol 3:1741‐1748, 2013.

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Figure 1. Figure 1. Primary hypertension arises from the interaction of genetic factors and the environmental factors of increased dietary NaCl intake and mental stress which increases efferent renal sympathetic nerve activity (ERSNA) resulting in a deficit in renal sodium excretory capacity.
Figure 2. Figure 2. Effects of increased renal sympathetic nerve activity (RSNA) on the 3 renal neuroeffectors: the juxtaglomerular granular cells (JGGC) with increased renin secretion rate (RSR) via stimulation of β‐1 adrenoceptors (AR), the renal tubular epithelial cells (T) with increased renal tubular sodium reabsorption and decreased urinary sodium excretion (UNaV) via stimulation of α‐1b AR, and the renal vasculature (V) with decreased RBF via stimulation of α‐1a AR. (Adapted, with permission, from reference 8).
Figure 3. Figure 3. Influence of renal nerves on relationship between urinary flow rate (%H2O excretion) or urinary sodium excretion (%Na excretion) and renal perfusion pressure (RPP). (Adapted, with permission, from reference 43).
Figure 4. Figure 4. The effect of air jet stress on renal sympathetic nerve activity (RSNA) and urinary sodium excretion (UNaV) in conscious WKY and SHR consuming either a normal or high NaCl diet. (Adapted, with permission, from reference 30)
Figure 5. Figure 5. The effect of prior renal denervation (DNX) on the response of urinary sodium excretion to air jet stress in conscious WKY and SHR consuming either a normal or high NaCl diet. (Adapted, with permission, from reference 30).
Figure 6. Figure 6. The evolution of mean arterial pressure (MAP, direct intra arterial recording) in borderline hypertensive rats (BHR) consuming either a 1% or 8% NaCl intake. After consuming 8% NaCl for 12 weeks (from week 6–week 18), the BHR 8% NaCl were switched back to 1% NaCl intake at week 18 and the evolution of MAP was examined for an additional 12 weeks.
Figure 7. Figure 7. In normotensive human subjects mental stress (color word test) increased mean arterial pressure (MAP) and heart rate (HR) but had no effect on renal plasma flow (RPF) and glomerular filtration rate (GFR). There was a significant decrease in urinary sodium excretion (UNaV) which was accompanied by an increase in fractional proximal tubular reabsorption (FPR) of sodium and water as measured by the lithium clearance technique. (Adapted, with permission, from reference 17).
Figure 8. Figure 8. The effect of changing from the supine to the standing position on renal vascular resistance in normotensive and borderline hypertensive (BHT) human subjects consuming either a low or a high NaCl diet. (Adapted, with permission, from reference 35).


Figure 1. Primary hypertension arises from the interaction of genetic factors and the environmental factors of increased dietary NaCl intake and mental stress which increases efferent renal sympathetic nerve activity (ERSNA) resulting in a deficit in renal sodium excretory capacity.


Figure 2. Effects of increased renal sympathetic nerve activity (RSNA) on the 3 renal neuroeffectors: the juxtaglomerular granular cells (JGGC) with increased renin secretion rate (RSR) via stimulation of β‐1 adrenoceptors (AR), the renal tubular epithelial cells (T) with increased renal tubular sodium reabsorption and decreased urinary sodium excretion (UNaV) via stimulation of α‐1b AR, and the renal vasculature (V) with decreased RBF via stimulation of α‐1a AR. (Adapted, with permission, from reference 8).


Figure 3. Influence of renal nerves on relationship between urinary flow rate (%H2O excretion) or urinary sodium excretion (%Na excretion) and renal perfusion pressure (RPP). (Adapted, with permission, from reference 43).


Figure 4. The effect of air jet stress on renal sympathetic nerve activity (RSNA) and urinary sodium excretion (UNaV) in conscious WKY and SHR consuming either a normal or high NaCl diet. (Adapted, with permission, from reference 30)


Figure 5. The effect of prior renal denervation (DNX) on the response of urinary sodium excretion to air jet stress in conscious WKY and SHR consuming either a normal or high NaCl diet. (Adapted, with permission, from reference 30).


Figure 6. The evolution of mean arterial pressure (MAP, direct intra arterial recording) in borderline hypertensive rats (BHR) consuming either a 1% or 8% NaCl intake. After consuming 8% NaCl for 12 weeks (from week 6–week 18), the BHR 8% NaCl were switched back to 1% NaCl intake at week 18 and the evolution of MAP was examined for an additional 12 weeks.


Figure 7. In normotensive human subjects mental stress (color word test) increased mean arterial pressure (MAP) and heart rate (HR) but had no effect on renal plasma flow (RPF) and glomerular filtration rate (GFR). There was a significant decrease in urinary sodium excretion (UNaV) which was accompanied by an increase in fractional proximal tubular reabsorption (FPR) of sodium and water as measured by the lithium clearance technique. (Adapted, with permission, from reference 17).


Figure 8. The effect of changing from the supine to the standing position on renal vascular resistance in normotensive and borderline hypertensive (BHT) human subjects consuming either a low or a high NaCl diet. (Adapted, with permission, from reference 35).
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Further Reading
 1. DiBona GF , Kopp UC . The neural control of renal function. Physiol Rev 77:76‐197, 1997
 2. Sever PS , Poulter NR A hypothesis for the pathogenesis of essential hypertension: The initiating factors. J Hypertens Suppl.7:S9‐S12, 1989.
 3. Esler M , Eikelis N , Schlaich M , Lambert G , Alvarenga M , Dawood T , Kaye D , Barton D , Pier C , Guo L , Brenchley C , Jennings G , Lambert E . Chronic mental stress is a cause of essential hypertension: Presence of biological markers of stress. Clin Exp Pharmacol Physiol 35:498‐502, 2008.
 4. Harshfield GA , Dong Y , Kapuku GK , Zhu H , Hanevold CD. Stress‐induced sodium retention and hypertension: A review and hypothesis. Curr Hypertens Rep 11:29–34, 2009.
 5. Johns EJ , Kopp UC , DiBona GF . Neural control of renal function. Compr Physiol 1:737‐767, 2011.

Further Reading

DiBona GF, Kopp UC. The neural control of renal function. Physiol Rev 77:76-197, 1997

Sever PS, Poulter NR A hypothesis for the pathogenesis of essential hypertension: the initiating factors. J Hypertens Suppl.7:S9-S12, 1989.

Esler M, Eikelis N, Schlaich M, Lambert G, Alvarenga M, Dawood T, Kaye D, Barton D, Pier C, Guo L, Brenchley C, Jennings G, Lambert E. Chronic mental stress is a cause of essential hypertension: presence of biological markers of stress. Clin Exp Pharmacol Physiol  35:498-502, 2008.

Harshfield GA, Dong Y, Kapuku GK, Zhu H, Hanevold CD. Stress-Induced Sodium Retention and Hypertension: A Review and Hypothesis. Curr Hypertens Rep 11:29–34, 2009.

Johns EJ, Kopp UC, DiBona GF. Neural control of renal function. Compr Physiol 1:737-767, 2011


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Gerald F. DiBona. Interaction of Stress and Dietary NaCl Intake in Hypertension: Renal Neural Mechanisms. Compr Physiol 2013, 3: 1741-1748. doi: 10.1002/cphy.c130010