Year : 1998 | Volume
: 9 | Issue : 1 | Page : 1--3
Salt and Hypertension in Man
Consultant Nephrologist, Bangalore Hospital, Bangalore, India
K S Ramprasad
Consultant Nephrologist, Bangalore Hospital, R.V. Road, Bangalore
|How to cite this article:|
Ramprasad K S. Salt and Hypertension in Man.Saudi J Kidney Dis Transpl 1998;9:1-3
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Ramprasad K S. Salt and Hypertension in Man. Saudi J Kidney Dis Transpl [serial online] 1998 [cited 2021 Aug 1 ];9:1-3
Available from: https://www.sjkdt.org/text.asp?1998/9/1/1/39292
History and Introduction
Salt has fascinated man from time immemorial. It has been referred to in ancient Arabic literature in the proverb "Salt in not worm-eaten" signifying its imperishable nature. Its importance in day to day life could be judged when a sixth century King said "one can do without gold but not without salt". It was believed that salt was essential to promote good health and the Latin works salus and salubris, which mean health and healthy are actually driven from sal (salt). Also, in ancient Rome, soldiers were paid in the form of salarium (salt money) from which today's "salary" is derived. Despite all these, the ancient Chinese in their wisdom noted in 3000 B.C., "if too much salt is used in food, the pulse hardens; tears make their appearance and the complexion changes". Today after nearly three millennia, we are still arguing over this statement.
Relation of Salt and Hypertension
Numerous reports, based on epidemiologic and demographic data, have pointed to the relationship between sodium intake and hypertension  . It seems likely that increased salt intake may be contributory but not sufficient cause for hypertension. Also, there is considerable heterogeneity of blood pressure response to salt intake  . Certain features such as African-American race and older age have been shown to be associated with increased salt sensitivity  . It has been shown that the hypertensive response to salt restriction is most prominent in patients with advanced disease  . Thus, the decline in blood pressure with salt restriction is small in patients with mild hypertension ,, and the full hypertensive response requires five weeks or more, and the factors responsible for the delay are not fully understood  .
The Intersalt Study  was conducted to investigate the correlation of blood pressure to sodium excretion in 52-countries worldwide. Based on the results of this study it was estimated that the systolic blood pressure should decline by 3.1 mm Hg in the general population for a decrease of 100 mmol of dietary salt. However, other studies such as the Scottish Health Study  failed to confirm this relationship. Many previous studies have also reported that dietary salt loading elevates blood pressure in some "salt sensitive" but all subjects , . However, De la Sieraa et al have demonstrated with 24 hours monitoring of blood pressure that the "salt resistance" individuals had higher sleeping blood pressures  .
Mechanism of Salt Sensitivity
The exact mechanism of salt sensitive hypertension is incompletely understood. There is evidence that hypertension results from a defect in the salt excretory capacity of the kidney , . Genetic factors such as alterations in structure or regulation of sodium transport in the nephron have been proposed  . Recently, it has been proposed that hypertension consists of two phases  . The first phase, which is mediated by a hyperactive sympathetic and rennin-angiotensin systems, results in elevation in blood pressure which is episodic. Elevation of blood pressure in such individuals may be viewed as physiologically appropriate, since the increase in renal perfusion pressure enhances sodium excretion and restores normovolemia. However, these repeated increases in blood pressure causes structural and functional adaptive responses in the kidney blunting its ability to excrete salt. This acquired defect in excreting salt results in salt-sensitive, persistent hypertension  .
Other factors that may contribute to salt sensitivity in hypertension include:
a) Selective activation of intra-renal angiotensin system leading to renal vasoconstriction and increased sodium reabsorption  .
b) Increases activity of the sodium-hydrogen exchanger which mediates a large portion of sodium reabsoption in the proximal tubule  .
c) Lack of occurrence of reduced sympathetic activity after salt intake  . This may partly be due to an outbain-like hormone released in the brain following high salt intake which may raise the blood pressure directly by increasing sympathetic outflow  .
d) Salt retention leads to release of a natriuretic hormone which causes inhibition of the Na-K-ATPase pump resulting in increases cell sodium concentration which in turn, diminishes passive sodium entry into the cells. This reduces the activity of sodium-calcium exchanger in the cell membrane resulting in an increase in intracellular calcium concentration. These changes in the vascular smooth muscle result in vasoconstriction and hypertension. Also, a high salt intake increases the excretion of calcium and the negative calcium balance thus created, may cause increased intra cellular calcium and vasoconstriction. This response is probably mediated by enhanced releases of parathyroid hormone and calcitriol  . This hypothesis is supported by the observation that a high calcium intake can minimize the saltinduced raise in blood pressure  .
e) Chloride also appears to be important since sodium when given alone or with another anion such as citrate does not result in value expansion and hypertension , .
The importance of salt restriction has come into focus in recent years due to its potential adverse effects including the demonstration that it can cause an elevation of LDL and total cholesterol levels  . Also, an association between low salt intake and myocardial infarction has been reported  . This may be because of the compensatory systems set into play by reducing salt intake, including increased rennin-angiotensin and sympathetic nervous system activity.
In conclusion, the relationship between salt intake and blood pressure is complex and susceptibility to salt induced hypertension in humans is variable. Although current studies indicate the need for modest restriction more objective studies on larger number of patients are needed to clarify the issue.
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