Superiority of salt restriction over diuretics in reducing renal hypertrophy and injury in uninephrectomized SHR

Benstein, Judith A.; Feiner, Helen; Parker, Miriam; Dworkin, Lance D.

doi:10.1152/ajprenal.1990.258.6.f1675

Cited by 49 publications

(47 citation statements)

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“…Similar prevention of proteinuria by dietary sodium restriction was previously described in uninephrectomized spontaneously hypertensive rats (3) and 5/6 nephrectomy model (10). In the latter studies (3,10), it was clearly shown that reduction in glomerular pressure determined by micropuncture or arterial pressure did not account for the beneficial effect of sodium restriction.…”

Section: Discussionmentioning

confidence: 97%

Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension

Rugale¹,

Delbosc

Cristol

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Rugale, Caroline, Sandrine Delbosc, Jean-Paul Cristol, Albert Mimran, and Bernard Jover. Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension. Am J Physiol Heart Circ Physiol 284: H1744-H1750, 2003. First published December 5, 2002 10.1152/ajpheart.00864.2002The influence of a low-sodium (LS) diet was assessed on the cardiac and renal alterations and pro-oxidant effect associated with a 10-day infusion of angiotensin II (200 or 400 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 , osmotic pumps). Tail-cuff pressure (TCP), albuminuria, and renal blood flow were determined at the end of the experiments. Heart weight index (HWI) and production of superoxide anion (O 2 Ϫ ⅐) by the left ventricle and H2O2 by the aorta was measured with the use of bioluminescence. Although the final TCP was similar in LS and normal sodium (NS) rats infused with high and low doses of angiotensin II, respectively, the increase in HWI was prevented by the LS diet. Sodium restriction reduced the rise in albuminuria without a change in the renal effect of angiotensin II. The increased production of O 2 Ϫ ⅐ and H2O2 observed in NS rats was abrogated in LS rats. The beneficial influence of dietary sodium restriction on target organ damage induced by angiotensin II is independent of arterial pressure reduction and possibly related to attenuation of the prooxidant effect of the peptide. heart weight; albuminuria; reactive oxygen species; renal hemodynamic THE DEVELOPMENT OF cardiac hypertrophy results from the interaction between several factors, including elevated arterial pressure, angiotensin II (ANG II), and sodium intake. Although blood pressure is an important determinant of cardiac mass (8), ANG II may directly increase protein synthesis and cause myocyte hypertrophy, as reported in cultured cardiac myocytes isolated from chicks (2) and neonatal rats (34). In vivo long-term administration of an initially subpressor dose of ANG II, a model that mimics the development of human hypertension, induces a gradual rise in blood pressure associated with a cardiac hypertrophy (7,14,17). However, ANG II might increase cardiac mass independently of arterial pressure. This was suggested by the presence of cardiac hypertrophy in rats infused with a nonpressor dose of the peptide (4, 37) or in rats infused with a pressor dose of ANG II and concomitantly treated by hydralazine (7, 37).The concentration of sodium ion in vitro or dietary sodium intake in vivo may modulate cardiac mass. In cultured neonatal rat myocardial myoblasts, cellular protein content and cell size increased when sodium concentration of the medium was augmented (15). In vivo, a high-sodium intake increased cardiac mass in normotensive rats (46) and exacerbated cardiac hypertrophy in hypertensive rats (12). In humans, sodium intake (assessed by urinary sodium excretion) and the left ventricular mass index were positively correlated in hypertensive and normotensive subjects (9). Conversely, a low-sodium (LS) intake prevents cardiac hypertrophy associated with two-k...

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Section: Discussionmentioning

confidence: 97%

Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension

Rugale¹,

Delbosc

Cristol

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…Dietary salt intake plays an important role not only in blood pressure but also in the progression of glomerular injury (20)(21)(22). Dahl-S rats are the most popular model of human salt-sensitive hypertension (23).…”

Section: Discussionmentioning

confidence: 99%

Enhancement of Glomerular Platelet-Derived Growth Factor β-Receptor Tyrosine Phosphorylation in Hypertensive Rats and Its Inhibition by Calcium Channel Blocker

et al. 2002

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“…In the uninephrectomised SHR salt restriction inhibits compensatory kidney growth. 59 In patients with hypertension an increase in salt intake often increases glomerular filtration rate, vascular resistance, calculated intraglomerular capillary pressure and protein excretion. 60 In normal humans the effect of a raised salt intake varies from no detectable effect or a decrease in renal vascular resistance, a few have a similar response to that which occurs in those hypertensive patients who have an increase in glomerular filtration.…”

Section: Renal Functionmentioning

confidence: 99%

Harmful effects of dietary salt in addition to hypertension

2002

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In addition to raising the blood pressure dietary salt is responsible for several other harmful effects. The most important are a number which, though independent of the arterial pressure, also harm the cardiovascular system. A high salt intake increases the mass of the left ventricle, thickens and stiffens conduit arteries and thickens and narrows resistance arteries, including the coronary and renal arteries. It also increases the number of strokes, the severity of cardiac failure and the tendency for platelets to aggregate. In renal disease, a high salt intake accelerates the rate of renal functional

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Superiority of salt restriction over diuretics in reducing renal hypertrophy and injury in uninephrectomized SHR

Cited by 49 publications

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Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension

Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension

Enhancement of Glomerular Platelet-Derived Growth Factor β-Receptor Tyrosine Phosphorylation in Hypertensive Rats and Its Inhibition by Calcium Channel Blocker

Harmful effects of dietary salt in addition to hypertension

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