[Sodium and hypertension].
Over several million years the human race was programmed to eat a diet which contained about 15 mmol of sodium (1 g of sodium chloride) per day. It is only five to ten thousand years ago that we became addicted to salt. Today we eat about 150 mmol of sodium (9-12 g of salt) per day. It is now apparent that this sudden rise in sodium intake (in evolutionary terms) is the most likely cause for the rise in blood pressure with age that occurs in the majority of the world's population. Those which consume less than 60 mmol/day do not develop hypertension. The reason for the rise in sodium intake is not known but it is probable that an important stimulus was the discovery that meat could be preserved by immersion into a concentrated salt solution. This seemingly miraculous power endowed salt with such magical and medicinal qualities that it became a symbol of goodness and health. It was not until 1904 Ambard and Beaujard suggested that on the contrary dietary salt could be harmful and raise the blood pressure. At first the idea did not prosper and it continues to be opposed by a diminishing band. The accumulated evidence that sodium intake is related to the blood pressure in normal man and animals and in inherited forms of hypertension has been obtained from experimental manipulations and studies of human populations. The following observation links sodium and hypertension. An increase in sodium intakes raises the blood pressure of the normal rat, dog, rabbit, baboon, chimpanzee and man. Population studies have demonstrated a significant correlation between sodium intake and the customary rise in blood pressure with age. The development of hypertensive strains of rats has revealed that the primary genetic lesion which gives rise to hypertension resides in the kidney where it impairs the urinary excretion of sodium. There is similar but less convincing evidence in essential hypertension. The kidney in both essential hypertension and hypertensive strains of rats share a number of functional abnormalities most of which are capable of impairing sodium excretion. Essential hypertension would appear to be as much a renal disturbance related to the intake of sodium as hypertension secondary to renal disease.
de Wardener
H E
HE
Department of Chemical Pathology, Charing Cross & Westminster Medical School, London.
D000328:Adult; D000367:Age Factors; D000818:Animals; D001794:Blood Pressure; D002417:Cattle; D004039:Diet, Sodium-Restricted; D004195:Disease Models, Animal; D004198:Disease Susceptibility; D004285:Dogs; D049672:History, 19th Century; D049673:History, 20th Century; D049690:History, Ancient; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000235:genetics / Q000503:physiopathology*; D007223:Infant; D007231:Infant, Newborn; D007676:Kidney Failure, Chronic / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009318:Natriuresis; D009747:Nutritional Physiological Phenomena; D002679:Pan troglodytes; D010215:Papio; D011817:Rabbits; D051381:Rats; D011918:Rats, Inbred SHR; D012982:Sodium, Dietary / Q000009:adverse effects / Q000266:history / Q000378:metabolism
D012982:Sodium, Dietary
Sodium et hypertension.