Dietary Fish Oil Prevents the Development of Renal Damage in Salt‐loaded Stroke‐prone Spontaneously Hypertensive Rats

Hobbs, Leanne M.; Rayner, Timothy E.; Howe, Peter R. C.

doi:10.1111/j.1440-1681.1996.tb02770.x

Cited by 16 publications

(15 citation statements)

References 30 publications

(1 reference statement)

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“…This finding is similar to the reported effects of FO in SHRs (44,87). However, as with blood pressure, urine protein excretion in SS ϩ HSD ϩ FO rats remained significantly elevated compared with that of the SR ϩ HSD rats.…”

Section: Discussionsupporting

confidence: 78%

“…In accord with several studies in SHRs (6,44,62,91), we demonstrate that FO prevents the development of chronic glomerular, tubulointerstitial, and vascular alterations in SS ϩ HSD rats. These extensive histopathological lesions were also observed in rats treated with HYD to lower blood pressure (SS ϩ HSD ϩ HYD).…”

Section: Discussionsupporting

confidence: 69%

“…Although we and others (6,44,62,91) have shown that FO decreases the development of renal injury in Dahl SS ϩ HSD rats, relatively few studies have addressed potential signaling pathways whereby FO confers a protective effect. In vitro studies of cultured cells treated with DHA or EPA have provided evidence for several potential signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

“…A number of studies have provided evidence that dietary fish oil (FO) supplementation ameliorates cardiovascular and renal disease in humans (12, 21-23, 38, 51, 68, 78, 92) and in a variety of experimental model systems, including spontaneously hypertensive rats (SHRs) (44,50,91) and Dahl salt-sensitive (SS) rats, which provide a model of human SS hypertension (45,83,85,86,94,101). Despite extensive study, potential mechanisms whereby dietary FO supplementation protects against the development of renal disease have not been adequately defined (33,34).…”

mentioning

confidence: 99%

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Signaling pathways modulated by fish oil in salt-sensitive hypertension

Díaz-Encarnación¹,

Warner²,

Gray³

et al. 2008

American Journal of Physiology-Renal Physiology

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Diaz Encarnacion MM, Warner GM, Gray CE, Cheng J, Keryakos HK, Nath KA, Grande JP. Signaling pathways modulated by fish oil in salt-sensitive hypertension. Am J Physiol Renal Physiol 294: F1323-F1335, 2008. First published April 2, 2008 doi:10.1152/ajprenal.00401.2007.-Although many studies have indicated that fish oil (FO) improves cardiovascular risk factors and reduces histopathological manifestations of injury in experimental renal injury models, potential mechanisms underlying this protective effect have not been adequately defined. The objective of this study was to identify potential signaling pathways that confer protection in the Dahl rat model of salt-sensitive hypertension. Male Dahl saltsensitive rats (n ϭ 10/group) were provided with formulated diets containing 8% NaCl, 20% protein, and 25% FO or 25% corn oil (CO) for 28 days. FO reduced blood pressure (Ϫ11% at 4 wk; P Ͻ 0.05), urine protein excretion (Ϫ45% at 4 wk; P Ͻ 0.05), plasma cholesterol and triglyceride levels (Ϫ54%, P Ͻ 0.001; and Ϫ58%, P Ͻ 0.05), and histopathological manifestations of renal injury, including vascular hypertrophy, segmental and global glomerular sclerosis, interstitial fibrosis, and tubular atrophy. Interstitial inflammation was significantly reduced by FO (Ϫ32%; P Ͻ 0.001), as assessed by quantitative analysis of ED1-positive cells in sections of the renal cortex. FO reduced tubulointerstitial proliferative activity, as assessed by Western blot analysis of cortical homogenates for PCNA (Ϫ51%; P Ͻ 0.01) and quantitative analysis of Mib-1-stained sections of the renal cortex (Ϫ42%; P Ͻ 0.001). Decreased proliferative activity was associated with reduced phospho-ERK expression (Ϫ37%; P Ͻ 0.005) and NF-B activation (Ϫ42%; P Ͻ 0.05). FO reduced cyclooxygenase (COX)-2 expression (Ϫ63%; P Ͻ 0.01) and membrane translocation of the NADPH oxidase subunits p47 phox and p67 phox (Ϫ26 and Ϫ34%; P Ͻ 0.05). We propose that FO ameliorates renal injury in Dahl salt-sensitive rats through the inhibition of ERK, decreased NF-B activation, inhibition of COX-2 expression, and decreased NADPH oxidase activation.fibrosis; glomerulosclerosis; docosahexaenoic acid; eicosapentaenoic acid; rat HYPERTENSIVE NEPHROSCLEROSIS is the second most common cause of end-stage renal disease in the United States (98). Over 70% of the 5.6 million individuals in the United States with elevated serum creatinine levels are hypertensive (16). The risk of end-stage renal disease is directly related to the degree of blood pressure elevation. Hypertension, which occurs in as many as 43 million individuals, is clearly a multifactorial disorder resulting from a variety of environmental and genetic factors. Of the environmental factors, excess dietary salt intake appears to be one of the most important (93, 103). Of note, salt sensitivity is an independent cardiovascular risk factor in patients with hypertension (69).Given the prevalence of hypertension, nontoxic, easily tolerated therapeutic agents that complement standard antihypertensive therapy may play a critical ...

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Section: Discussionsupporting

confidence: 78%

Section: Discussionsupporting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Signaling pathways modulated by fish oil in salt-sensitive hypertension

Díaz-Encarnación¹,

Warner²,

Gray³

et al. 2008

American Journal of Physiology-Renal Physiology

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“…The SHRSP rat model used in the present study is a widely used model for hemorrhagic stroke and essential hypertension (31)(32)(33). In this model, the FA composition of dietary fats had no major influence on the development of hemorrhagic stroke and life span of SHRSP rats, in contrast to models of cardiovascular diseases (21,22,(34)(35)(36). In humans also, a recent epidemiological study showed that the risk of developing hemorrhagic stroke is not associated with dietary levels of MUFA and PUFA (37).…”

Section: Discussionmentioning

confidence: 98%

Comparative health effects of margarines fortified with plant sterols and stanols on a rat model for hemorrhagic stroke

Ratnayake

Plouffe

L’Abbé

et al. 2003

Lipids

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There is increased acceptance of fortifying habitual foods with plant sterols and their saturated derivatives, stanols, at levels that are considered safe. These sterols and stanols are recognized as potentially effective dietary components for lowering plasma total and LDL cholesterol. Our previous studies have shown that daily consumption of plant sterols promotes strokes and shortens the life span of stroke-prone spontaneously hypertensive (SHRSP) rats. These studies question the safety of plant sterol additives. The present study was performed to determine whether a large intake of plant stanols would cause nutritional effects similar to those seen with plant sterols in SHRSP rats. Young SHRSP rats (aged 26-29 d) were fed semipurified diets containing commercial margarines fortified with either plant stanols (1.1 g/100 g diet) or plant sterols (1.4 g/100 g diet). A reference group of SHRSP rats was fed a soybean oil diet (0.02 g plant sterols/100 g diet and no plant stanols). Compared to soybean oil, both plant stanol and plant sterol margarines significantly (P < 0.05) reduced the life span of SHRSP rats. At the initial stages of feeding, there was no difference in the survival rates between the two margarine groups, but after approximately 50 d of feeding, the plant stanol group had a slightly, but significantly (P < 0.05), lower survival rate. Blood and tissue (plasma, red blood cells, liver, and kidney) concentrations of plant sterols in the plant sterol margarine group were three to four times higher than the corresponding tissue concentrations of plant stanols in the plant stanol group. The deformability of red blood cells and the platelet count of SHRSP rats fed the plant sterol margarine were significantly (P < 0.05) lower than those of the plant stanol margarine and soybean oil groups at the end of the study. These parameters did not differ between the soybean oil and plant stanol margarine groups. These results suggest that, at the levels tested in the present study, plant stanols provoke hemorrhagic stroke in SHRSP rats to a slightly greater extent than plant sterols. The results also suggest that the mechanism by which plant stanols shorten the life span of SHRSP rats might differ from that of plant sterols.

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n-3 Polyunsaturated fatty acids in the treatment of patients with IgA nephropathy

Grande

Donadío

1998

Medicinal Fatty Acids in Inflammation

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Dietary Fish Oil Prevents the Development of Renal Damage in Salt‐loaded Stroke‐prone Spontaneously Hypertensive Rats

Cited by 16 publications

References 30 publications

Signaling pathways modulated by fish oil in salt-sensitive hypertension

Signaling pathways modulated by fish oil in salt-sensitive hypertension

Comparative health effects of margarines fortified with plant sterols and stanols on a rat model for hemorrhagic stroke

n-3 Polyunsaturated fatty acids in the treatment of patients with IgA nephropathy

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