A review of long-term effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol and triglyceride

1. Dose—response curves for the pressor activity of angiotensin II have been determined in unanaesthetized rats receiving diets containing 2·5% (w/w) or 0·007% (w/w) sodium; the different diets were administered in various sequences. 2. In comparison with those from rats receiving a low sodium diet, the dose—response curves were displaced to the left on the high sodium diet, indicating a greater response to angiotensin, and this displacement persisted for a period of approximately 7 days after the diet was changed from high to low sodium. The dose—response curve subsequently shifted to the right when the low sodium diet was maintained for longer. 3. There was a negative correlation between the slope of the dose—response curve and the basal blood pressure in all groups; the correlation was significant in three out of the five different treatment groups. 4. Basal blood pressures were significantly raised in rats on the high sodium diet for 7 days. 5. A number of possible mechanisms have been considered to explain both the parallel shift of the dose—response curve and alteration in its slope. It is concluded that the observed findings are compatible with an action of sodium-loading on the sensitivity of the smooth muscle cell to angiotensin, on the resting of the renin—angiotensin system, on the rate of in-activation of angiotensin and on a change in initial length of the muscle fibre.

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Endogenous angiotensin modulates PGE2-mediated release of substance P from renal mechanosensory nerve fibers

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2002.282.1.r19 ◽

2002 ◽

Vol 282 (1) ◽

pp. R19-R30 ◽

Cited By ~ 13

Author(s):

Ulla C. Kopp ◽

Michael Z. Cicha ◽

Lori A. Smith

Keyword(s):

Substance P ◽

Nerve Fibers ◽

Ang Ii ◽

High Sodium ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium ◽

Pelvic Perfusion ◽

High Sodium Diet ◽

Pelvic Pressure

Increasing renal pelvic pressure increases afferent renal nerve activity (ARNA) by a prostaglandin E2(PGE2)-mediated release of substance P (SP) from renal pelvic sensory nerves. We examined whether the ARNA responses were modulated by high- and low-sodium diets. Increasing renal pelvic pressure resulted in greater ARNA responses in rats fed a high-sodium than in those fed a low-sodium diet. In rats fed a low-sodium diet, increasing renal pelvic pressure 2.5 and 7.5 mmHg increased ARNA 2 ± 1 and 13 ± 1% before and 12 ± 1 and 22 ± 2% during renal pelvic perfusion with 0.44 mM losartan. In rats fed a high-sodium diet, similar increases in renal pelvic pressure increased ARNA 10 ± 1 and 23 ± 3% before and 1 ± 1 and 11 ± 2% during pelvic perfusion with 15 nM ANG II. The PGE2-mediated release of SP from renal pelvic nerves in vitro was enhanced in rats fed a high-sodium diet and suppressed in rats fed a low-sodium diet. The PGE2 concentration required for SP release was 0.03, 0.14, and 3.5 μM in rats fed high-, normal-, and low-sodium diets. In rats fed a low-sodium diet, PGE2increased renal pelvic SP release from 5 ± 1 to 6 ± 1 pg/min without and from 12 ± 1 to 21 ± 2 pg/min with losartan in the incubation bath. Losartan had no effect on SP release in rats fed normal- and high-sodium diets. ANG II modulates the responsiveness of renal pelvic mechanosensory nerves by inhibiting PGE2-mediated SP release from renal pelvic nerve fibers.

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Recovery from acute renal failure predisposes hypertension and secondary renal disease in response to elevated sodium

AJP Renal Physiology ◽

10.1152/ajprenal.00279.2006 ◽

2007 ◽

Vol 293 (1) ◽

pp. F269-F278 ◽

Cited By ~ 76

Author(s):

Kimberly R. Spurgeon-Pechman ◽

Deborah L. Donohoe ◽

David L. Mattson ◽

Hayley Lund ◽

Leilani James ◽

...

Keyword(s):

Renal Failure ◽

Acute Renal Failure ◽

Renal Disease ◽

Ischemia Reperfusion ◽

Salt Diet ◽

High Sodium ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium ◽

High Sodium Diet

Recovery of renal function is a well-characterized feature of models of acute renal failure; however, more recent studies have reported a predisposition to chronic renal disease. This study sought to determine the susceptibility to sodium-dependent hypertension following recovery from ischemic acute renal failure. Following ischemia-reperfusion (I/R) injury, rats were allowed to recover for 35 days on a 0.4% salt diet, then were switched to 4.0% salt diet for an additional 28 days. Blood pressure was significantly increased in postischemic rats switched to high-sodium diet at day 35 (19 ± 9 mmHg) compared with postischemic rats maintained on low-sodium diet. Plasma renin activity and creatinine clearance were not affected by I/R injury. The ischemic injury combined with transfer to 4.0% salt diet resulted in marked renal hypertrophy characterized by interstitial cellular deposition, tubular dilation, and enhanced rates of albumin excretion. Glomerular structure was altered in post-I/R rats switched to high-sodium diet but not in those maintained on low-sodium diets. When rats were acclimated to high-sodium diet before I/R injury, the early injury was similar to that observed in animals acclimated to low-sodium diet, and these animals progressed rapidly toward chronic kidney disease, as evidenced by advancement of albuminuria. These data suggest that the recovery from acute I/R injury is not complete, compromises Na homeostasis, and predisposes hypertension and secondary renal disease.

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