Chronic Sodium Chloride Toxicity in the Albino Rat. III. Maturity Characteristics, Survivorship, and Organ Weights

Tucker, Robert G.; Ball, C. Olin; Darby, William J.; Early, Walter R.; Kory, Ross C.; Youmans, John B.; Meneely, George R.

doi:10.1093/geronj/12.2.182

Cited by 19 publications

(7 citation statements)

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“…67 In contrast with the early appearance of cardiac hypertrophy in rats exposed to very high salt levels, cardiac weights in the 2.8% NaCl group remained normal until the later stages of life, with cardiac hypertrophy becoming evident only among rats surviving for at least 20 months. Similarly, the effect on mortality was also delayed in the 2.8% NaCl group, becoming evident only after B16 months of age, whereas mortality occurred earlier at higher salt levels.…”

Section: Progressive Salt-induced Hypertensionmentioning

confidence: 83%

“…[65][66][67] In their experiments, the effects of dietary salt were investigated in more than 600 male outbred (Sprague-Dawley) rats followed over their lifespan (up to 30 months). Although many levels of dietary salt were investigated, results obtained for a moderately high salt (2.8% NaCl) diet and control (0.15% NaCl) diet are of particular relevance.…”

Section: Progressive Salt-induced Hypertensionmentioning

confidence: 99%

“…The 2.8% NaCl diet was considered to be roughly comparable with a 14 g NaCl (240 mmol Na) intake in humans (assuming a 500 g dry weight daily food intake). [65][66][67] Such an intake is above the average sodium intake in Western societies but nevertheless corresponds with the normal level of sodium intakes in many individuals (for example, it corresponds with the sodium intake of X5% of the American population as a whole and with the intake of B25% of young American male individuals 18 ). Using the same assumptions, the 0.15% NaCl control diet corresponds with a 0.75 g NaCl (13 mmol Na) intake; that is, within the range of levels found in huntergatherer societies.…”

Section: Progressive Salt-induced Hypertensionmentioning

confidence: 99%

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The time course of salt-induced hypertension, and why it matters

Vliet

Montani

2008

Int J Obes

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The epidemiology of salt-induced hypertension has been explored in detail in animal studies, in some cases involving exposures to excess dietary salt for much of the animal's lifespan. The results of these studies demonstrate the presence of two distinct time courses of the blood pressure response to a high salt intake: an acute (rapid) blood pressure response occurring over days to weeks, and a slow and progressive blood pressure response that develops over extremely long periods of time, amounting to a significant fraction of the lifespan in normal individuals. The acute form of salt sensitivity is well known in humans, having often been demonstrated as a fall in blood pressure during the period of salt restriction. The slow and progressive form of salt sensitivity has been demonstrated directly in rats and chimpanzees and is also evident in analyses of human cross-population data as a salt dependency of age-associated changes of blood pressure. This slow and progressive component of salt-induced hypertension may be attributable, at least in part, to a progressive rise in the acute salt sensitivity of blood pressure during sustained exposure to high salt. However, a progressively irreversible or 'self sustaining' component of salt-induced hypertension has also been demonstrated in rat studies. This irreversible component has not been completely characterized, but its presence raises the possibility that blood pressure responses to salt restriction may not fully reveal the contribution of salt to blood pressure or the epidemiology of hypertension. These various components of salt sensitivity (acute vs slow, reversible vs irreversible) should be considered in any comprehensive explanation of the effects of salt on blood pressure and especially in experimental studies of the genetic and physiological mechanisms underlying salt-induced hypertension.

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Section: Progressive Salt-induced Hypertensionmentioning

confidence: 83%

Section: Progressive Salt-induced Hypertensionmentioning

confidence: 99%

Section: Progressive Salt-induced Hypertensionmentioning

confidence: 99%

See 1 more Smart Citation

The time course of salt-induced hypertension, and why it matters

Vliet

Montani

2008

Int J Obes

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“…While no direct causal relation is demonstrated between high hypertension and excess total body sodium, the association is strong, and one cannot well resist the temptation to link them in a working hypothesis, as have others from different kinds of data. 14 The great prolongation of life brought about by adding potassium at lower levels of high salt feeding cannot be explained on the basis of preventing the "benign essential hypertension" seen among the 2.8 and the 5.6% salt rats. The rationalization offered in the introduction to this presentation appeals to us.…”

Section: Resultsmentioning

confidence: 99%

Chronic Sodium Chloride Toxicity: The Protective Effect of Added Potassium Chloride

1957

Ann Intern Med

101

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EARLY in our investigations of chronic sodium chloride toxicity, possible interrelations between dietary sodium and potassium came to our attention. There has been a good basis for suspecting such since 1843. At that time it was suggested, on the basis of direct chemical analysis, that the herbivores' need for salt and the occasion for their long journeys in search of it were due not to lack of sodium in the diet but to an excess of potassium. We drew attention to this in introductory remarks to our presentations before the September, 1952, meeting of the American Physiological Society. 1 ' 2 These remarks were subsequently embodied in an editorial in 1954. 3 It would seem, then, that the greater potassium content of the herbivorous diet rather than its smaller salt content was the reason for the herbivores' great treks to salt licks. Carnivores, on the other hand, apparently acquire the salt they need from their natural diet, i.e., the flesh of other animals.Unquestionably the finest and greatest of all physiologic experiments was Claude Bernard's with a single rabbit, accomplished all within six weeks. From it flowed the entire concept of endogenous as different from exogenous metabolism. For two weeks he fed the rabbit vegetables. It passed a cloudy alkaline urine. For two weeks he fed the rabbit meat. It passed a clear acid urine. For the final two weeks he fed the rabbit nothing. It passed a clear acid urine. From this he concluded the rabbit was eating meat during that last two weeks. Rabbit meat. Think now also about fera naturae, their medical and surgical emergencies. 4 If a saber-toothed tiger (figure 1) encountered a woolly mammoth apt with his tusks he might come out of the affair with a real "Saturday night" set of contusions, lacerations and fractures. He would lie where he fell, or at best nearby where he could crawl. Whether he lived or died would then depend entirely upon the physiologic resources built into him for the emergency by eons of evolution due to

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“…This is well exemplified by a series of studies carried out by a group of investigtors at Vanderbilt University during the mid 1950's and early 1960's (45, [66][67][68]106). They varied the salt and potassium content of standard basal maintenance diets (see cited publications) which they fed to large numbers of Sprague-Dawley rats and later to Beagle dogs.…”

Section: Dietary Factorsmentioning

confidence: 99%