Effect of variations in dietary sodium intake on sodium excretion in mature rats

Brensilver, Jeffrey M.; Daniels, Frederick H.; Lefavour, Gertrude S.; Malseptic, Ronald M.; Lorch, Jonathan A.; Ponte, Melvin L.; Cortell, Stanley

doi:10.1038/ki.1985.38

Cited by 23 publications

(8 citation statements)

References 30 publications

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“…Mice were fed either a LS diet containing 0.15% sodium chloride or chow containing a standard sodium concentration (NaCl 1.27%), i.e., a NS diet. The LS groups were fed the minimum amount of sodium chloride required for a normal rodent growth rate [ 16 ]. Individual animal body weight and group chow intake follow-up started after weaning, and these parameters were monitored three times per week until the end of the experiment.…”

Section: Methodsmentioning

confidence: 99%

Low-sodium diet induces atherogenesis regardless of lowering blood pressure in hypertensive hyperlipidemic mice

et al. 2017

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This study investigated the influence of sodium restriction and antihypertensive drugs on atherogenesis utilizing hypertensive (H) low-density lipoprotein-receptor knockout mice treated or not with losartan (Los) or hydralazine (Hyd) and fed low-sodium (LS) or normal-sodium (NS) chow. Despite reducing the blood pressure (BP) of H-LS mice, the LS diet caused arterial lipid infiltration due to increased plasma total cholesterol (TC) and triglycerides (TG). Los and Hyd reduced the BP of H-LS mice, and Los effectively prevented arterial injury, likely by reducing plasma TG and nonesterified fatty acids. Aortic lipid infiltration was lower in Los-treated H-LS mice (H-LS+Los) than in normotensive (N)-LS and H-LS mice. Aortic angiotensin II type 1 (AT1) receptor content was greater in H-NS than H-LS mice and in H-LS+Hyd than H-LS+Los mice. Carboxymethyl-lysine (CML) and receptor for advanced glycation end products (RAGE) immunostaining was greater in H-LS than H-NS mice. CML and RAGE levels were lower in LS animals treated with antihypertensive drugs, and Hyd enhanced the AT1 receptor level. Hyd also increased the gene expression of F4/80 but not tumor necrosis factor-α, interleukin (IL)-1β, IL-6, IL-10, intercellular adhesion molecule-1 or cluster of differentiation 66. The novelty of the current study is that in a murine model of simultaneous hypertension and hyperlipidemia, the pleiotropic effect of chronic, severe sodium restriction elicited aortic damage even with reduced BP. These negative effects on the arterial wall were reduced by AT1 receptor antagonism, demonstrating the influence of angiotensin II in atherogenesis induced by a severely LS diet.

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Section: Methodsmentioning

confidence: 99%

Low-sodium diet induces atherogenesis regardless of lowering blood pressure in hypertensive hyperlipidemic mice

et al. 2017

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“…A more meaningful approach for comparing Na + intakes may be to consider the experimental intakes reached in rats and humans relative to the physiological Na + requirement for each species. The minimal physiological need for Na + in rats is somewhat controversial, but Brensilver et al [61] has estimated that a minimal Na + intake of approximately 0.25 mmol/day is required to sustain normal growth if caloric intake is sufficient. Taking into account the range of Na + contents for diets used in the rat studies cited above, and assuming that adult male Sprague-Dawley rats (typically used in these studies) consume 20-30 g of food per day [62,63], estimated Na + intake would range from 0.34 to 4.17 mmol/day for animals consuming the low salt diets and from 13.9 to 41.8 mmol/day for animals consuming the high salt diets.…”

Section: Human Studiesmentioning

confidence: 99%

The Effect of High Salt Intake on Endothelial Function: Reduced Vascular Nitric Oxide in the Absence of Hypertension

Boegehold¹

2013

J Vasc Res

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Within the last 25 years, it has become increasingly clear that high dietary salt intake represents a risk factor for the development of cardiovascular disease that is independent of its well-known ability to increase arterial pressure in some individuals. Studies in normotensive experimental animals and human subjects have revealed that a key feature of this pressure-independent effect of dietary salt is a profound reduction in vascular nitric oxide (NO) bioavailability that limits endothelium-dependent dilation. This reduction in NO is strongly associated with increased levels of reactive oxygen species (ROS) generated by NAD(P)H oxidase, xanthine oxidase or uncoupled endothelial NO synthase within the vascular wall, leading not only to scavenging of NO but also to disruption of some signaling pathways that mediate its production. The mechanistic link between high salt intake and elevated levels of enzymatically generated ROS in the peripheral vasculature is not clear, but a reduction in circulating angiotensin II may play a key role in this regard. Additional studies are needed to further elucidate the mechanisms, both at the systemic level and within the vascular wall, that trigger these salt-induced deficits in endothelial function, and to further clarify how the attendant loss of NO may disrupt tissue blood flow regulation and ultimately lead to adverse cardiovascular events.

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“…LSD groups were fed the minimum sodium chloride required for a normal rodent growth rate (20). Because experiments were time consuming and prolonged sample storage imposed technical constraints on some analyses, such as blood NEFA, urinary ions, and aortic histology, studies were carried out in batches of approximately six animals each.…”

Section: Experimental Protocolsmentioning

confidence: 99%

Dietary sodium chloride restriction enhances aortic wall lipid storage and raises plasma lipid concentration in LDL receptor knockout mice

Catanozi

Rocha

Passarelli

et al. 2003

Journal of Lipid Research

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This study aimed at measuring the influence of a low salt diet on the development of experimental atherosclerosis in moderately hyperlipidemic mice. Experiments were carried out on LDL receptor (LDLR) knockout (KO) mice, or apolipoprotein E (apoE) KO mice on a low sodium chloride diet (LSD) as compared with a normal salt diet (NSD). On LSD, the rise of the plasma concentrations of TG and nonesterified fatty acid (NEFA) was, respectively, 19% and 34% in LDLR KO mice, and 21% and 35% in apoE KO mice, and that of plasma cholesterol was limited to the LDLR KO group alone (15%). Probably due to the apoE KO severe hypercholesterolemia, the arterial inner-wall fat storage was not influenced by the diet salt content and was far more abundant in the apoE KO than in the LDLR KO mice. However, in the less severe hypercholesterolemia of the LDLR KO mice, lipid deposits on the LSD were greater than on the NSD. Arterial fat storage correlated with NEFA concentrations in the LDLR KO mice alone (n ‫؍‬ 14, P ‫؍‬ 0.0065).Thus, dietary sodium chloride restriction enhances aortic wall lipid storage in moderately hyperlipidemic mice.

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Effect of variations in dietary sodium intake on sodium excretion in mature rats

Cited by 23 publications

References 30 publications

Low-sodium diet induces atherogenesis regardless of lowering blood pressure in hypertensive hyperlipidemic mice

Low-sodium diet induces atherogenesis regardless of lowering blood pressure in hypertensive hyperlipidemic mice

The Effect of High Salt Intake on Endothelial Function: Reduced Vascular Nitric Oxide in the Absence of Hypertension

Dietary sodium chloride restriction enhances aortic wall lipid storage and raises plasma lipid concentration in LDL receptor knockout mice

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