Blood Pressure, Cholesterol Content of Serum and Tissues, and Atherogenesis in the Rat

Deming, Quentin B.; Mosbach, Erwin H.; Bevans, Margaret; Daly, Marie M.; Abell, Liese L.; Martin, E.; Brun, L. M.; Halpern, Ellen L.; Kaplan, R.

doi:10.1084/jem.107.4.581

Cited by 63 publications

(10 citation statements)

References 6 publications

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“…Deming et al (22), in studying the effect of experimental hypertension on atherogenesis in the rat, concluded that among animals on an atherogenic diet there was a positive correlation between elevation in blood pressure and serum cholesterol concentration. In attempting to assess the role of salt as distinct from that of desoxycorticosterone they concluded that salt was without effect on plasma lipids.…”

Section: Discussionmentioning

confidence: 99%

“…At the present time, we are aware of no evidence which would suggest that salt plays a role in atherogenesis either in experimental animals or man. Indeed, in the experimental studies of atherosclerosis alluded to above (19,22,23) the authors noted specifically that the excess salt ingestion failed to increase the atherosclerotic lesions. Nonetheless, if excessive salt ingestion is capable of elevating plasma lipids it may conceivably affect atherogenesis as well.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Chronic Excess Salt Feeding

Dahl

1960

The Journal of Experimental Medicine

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The interrelationship of hypertension and atherosclerosis has been the subject of repeated investigation and a voluminous literature. At the present time it is generally thought that there is no basic etiological relationship between the two diseases; however, it appears that hypertension accelerates the progress of established atherosclerosis and that the inception of atherosclerosis is hastened by the presence of antecedent hypertension (1).For some years we have been studying the effects of chronic excess salt feeding in man and animals in an effort to explore the etiologic relationship between salt ingestion and human essential hypertension (2-5). We recently concluded such a study on dogs and rats. The results suggest that chronic salt ingestion is capable of elevating the concentration of plasma lipids. The available evidence is insufficient to conclude that such a factor operates in man to raise plasma lipid levels or that it is involved in the production of atherosclerosis, either human or experimental. Nonetheless, since salt has been invoked in the pathogenesis of human hypertension (4), the present studies suggest one possible biochemical basis for a link between atherosclerosis and hypertension. EXPERIMENTAL Animals and Feeding Programs:1. Rats.--All animals were Sprague-Dawley females. Group I consisted of 16 animals of which 11 were salt-fed and 5 were controls; salt feeding was begun at age 21/~ months and continued up to the time of sacrifice, more than 15 months later. Group II included 41 animals, 11 controls and 15 on each of the two salt regimens described below; salt feeding was started at age 1 month and blood for cholesterols was obtained 6~ months later. Group III with 36 animals, of which 12 were controls, was similar to Group II except that salt feeding began at 3 weeks of age and blood for cholesterols was obtained 8 weeks later, All animals were housed in air-conditioned rooms, 2 to 6 animals per cage, and were allowed free access to drinking (tap) water and food. Repeated analyses of the tap water showed it to contain only 0.5 to 0.7 m.eq. of sodium per liter. The basic diet that all control animals received in unmodified form was Ralston Purina fox chow pellets, which by our analyses contained sodium in amounts ranging from 0.51 to 0.74 per cent calculated as NaC1.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of Chronic Excess Salt Feeding

Dahl

1960

The Journal of Experimental Medicine

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“…A previous report showed that rats will develop atherosclerotic lesions when maintained on the latter diet (13), but in the present study, rats were sacrificed before they had developed gross atherosclerotic lesions in the aorta.…”

Section: Discussionmentioning

confidence: 99%

Cholesterol Concentration and Cholesterol Synthesis in Aortas of Rats With Renal Hypertension*

Daly¹,

Deming²,

Raeff³

et al. 1963

J. Clin. Invest.

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Hypertension has been shown to increase the severity of atherosclerosis in both man and experimental animals (1). Most observers attribute this effect of hypertension to local damage to the vessels produced by the augmented pressure or turbulence of the blood. This concept is supported by the more frequent occurrence and greater severity of atherosclerotic lesions at locations of high pressure or turbulence. It has also been suggested that high blood pressure increases the filtration of blood across arterial walls and, presumably, affords an opportunity for retention of lipid in the walls (2).The present report is concerned with two other factors that may affect the concentration of lipid in the aortas of hypertensive rats: the concentration of lipid in the blood, and lipid synthesis in the aorta itself. Cholesterol concentrations were found to be significantly higher in aortas of hypertensive rats than in those of normotensive controls. This difference was observed when hypertensive animals had higher serum cholesterol levels than their controls, but the difference persisted when experimental conditions were adjusted so that the serum cholesterol levels were comparable in the two groups of animals. It was found that the rate of cholesterol synthesis in vitro is increased in the aortas of hypertensive rats. A Gaertner cuff 22 mm long 'and an "Infraton" 4 pickup were used.Parabiotic pairs. Wistar rats were inbred in this laboratory by mating siblings for at least ten generations; CFN rats were inbred in the same way for three generations. Parabiotic pairs were prepared by suturing the previously divided lateral abdominal musculature of the two rats while maintaining separation of the peritoneal cavities and joining the scapulae.Cholesterol concentration in serum. To obtain blood for the measurement of serum cholesterol levels at intervals, rats under light ether anesthesia were bled by

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“…(19). At that time, earlier studies by others in the chicken (42), rat (43), and rabbit (44) furnished no support for this hypothesis. Subsequently, however, it was reported (45) that the incidence of myocardial and renal infarcts as well as the deposition of fat in the aortas of rats on an atherogenic diet were increased when 1-2 % saline replaced tap water for drinking, without associated changes in blood pressure.…”

Section: Inmentioning

confidence: 89%

FURTHER EVIDENCE OF THE TOXICITY OF NaCl

Dahl

Tuthill

1974

The Journal of Experimental Medicine

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There are now three strains of hypertension-prone rats in which genetic factors are demonstrably involved in setting average blood pressure levels. The first strain was described by Smirk and Hall in 1958 (1), the second by Dahl et al. in 1962 (2, 3), and the third by Okamoto and Aoki in 1963 (4). Formal genetic studies indicated that blood pressure control was multigenic in all three strains (5-7). It is likely that these strains share some genes that control blood pressure but the available evidence is not consistent with the possibility that they share them all. Among a number of differences in these strains that suggest nonidentity of the gene pools controlling blood pressure, none is more evident than the response to excess dietary salt (NaC1). Both the New Zealand strain isolated by Smirk and Hall (1) and the spontaneously hypertensive rat (SHR) 1 separated by Okamoto and Aoki (4) develop significant hypertension without additional dietary salt, whereas the sensitive strain developed by Dahl et al. (2, 3) was originally evolved specifically on the basis of its hypertensive response to NaC1. The fact that some rats develop hypertension spontaneously on normal salt intakes led to the widespread belief that salt intake was therefore unimportant. In the aggregate, our long experience studying both clinical and experimental hypertension by modifying dietary NaC1 is incompatible with such a concept. The belief that dietary NaC1 is unimportant if elevations in blood pressure are insignificantly affected by increments or decrements in salt consumption represents, in our opinion, a simplistic view of such a lethal disease as hypertension. If there is evidence of increased mortality in association with increased salt intake or decreased mortality with decreased salt intake, whatever the effects on blood pressure, this is of consequence: the importance of survival in considerations affecting one of the major cardiovascular diseases is not to be underrated.The present work was done as part of a continuing long-term study in which the relative importance of dietary NaC1 and genetic makeup are being evaluated, in a variety of situations, in both clinical and experimental hypertension.

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Blood Pressure, Cholesterol Content of Serum and Tissues, and Atherogenesis in the Rat

Cited by 63 publications

References 6 publications

Effects of Chronic Excess Salt Feeding

Effects of Chronic Excess Salt Feeding

Cholesterol Concentration and Cholesterol Synthesis in Aortas of Rats With Renal Hypertension*

FURTHER EVIDENCE OF THE TOXICITY OF NaCl

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