Role of the renin-angiotensin system in the adaptation of aldosterone biosynthesis to sodium restriction in the rat

Tarján, É.; Spät, András; Balla, Tamás; Székely, Annamária

doi:10.1530/acta.0.0940381

Cited by 14 publications

(8 citation statements)

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“…As expected, the LSD group presented a significant reduction of urinary excretion of sodium, fractional excretion of sodium, and osmolarity. This reduction in sodium excretion was accompanied by an important elevation of serum aldosterone, a result of the well-known activation of the RAAS during sodium restriction, as extensively reported by other authors (Tarjan et al 1980;Rubattu et al 1994;Jo et al 1996).…”

Section: Resultssupporting

confidence: 75%

Upregulation and intrarenal redistribution of heat shock proteins 90α and 90β by low-sodium diet in the rat

Ramírez¹,

Uribe²,

García-Torres³

et al. 2004

Cell Stress Chaper

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Two genes encoding isoforms heat shock protein (Hsp) 90alpha and Hsp90beta constitute the Hsp90 subfamily. In addition to their role in regulating mineralocorticoid and glucocorticoid receptors, these proteins have been associated with nitric oxide production. However, little is known regarding Hsp90 isoform expression and regulation in kidney. In this study we characterized the expression and localization of Hsp90 isoforms and evaluated the influence of low-sodium intake on their expression and distribution in kidney by using reverse transcription-polymerase chain reaction, Western blot, and immunohistochemistry techniques. We found that Hsp90alpha and Hsp90beta were expressed abundantly in both the renal cortex and the medulla; however, Hsp90 isoform expression was higher in the medulla than in the cortex. Immunohistochemistry of Hsp90alpha and Hsp90beta showed intense staining in the apical membrane of proximal and distal tubules. In the outer cortex these proteins were localized intracytosolically, whereas in the inner renal medulla they were restricted mainly to the basolateral membrane. Expression of Hsp9alpha and Hsp90beta was upregulated in the renal cortex during sodium restriction. In addition, both proteins exhibited redistribution from the cytoplasm to the basolateral side in thick ascending limb cells when rats were fed with a low-salt diet. Our results showed that Hsp90alpha and Hsp90beta were expressed abundantly in renal tissue. Expression and localization patterns under normal and salt-restricted intake were different between the cortex and the medulla, suggesting that these proteins may be involved in different processes along the nephron. Hsp90alpha and Hsp90beta upregulation induced by a low-sodium diet together with redistribution in thick ascending limb cells suggests that Hsp90 plays a role in the modulation of sodium reabsorption under these circumstances.

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Section: Resultssupporting

confidence: 75%

Upregulation and intrarenal redistribution of heat shock proteins 90α and 90β by low-sodium diet in the rat

Ramírez¹,

Uribe²,

García-Torres³

et al. 2004

Cell Stress Chaper

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“…infusion49–51; however, most reports utilizing rats suggest that changes in salt intake do not significantly affect plasma sodium concentration (e.g. Refs. 52–54).…”

Section: Effects Of Increased Salt Intake On the Sympathetic Nervous mentioning

confidence: 99%

The Interaction of Angiotensin II and Osmolality in the Generation of Sympathetic Tone during Changes in Dietary Salt Intake

Brooks

Scrogin

McKeogh

2001

Annals of the New York Academy of Sciences

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At rest, sympathetic nerves exhibit tonic activity which contributes to arterial pressure maintenance. Significant evidence suggests that the absolute level of sympathetic tone is altered in a number of physiologic and pathophysiologic states. However, the mechanisms by which such changes in sympathetic tone occur are incompletely understood. The purpose of this review is to present evidence that humoral factors are essential in these changes and to detail specifically an hypothesis for the mechanisms that underlie the changes in sympathetic tone that are produced during increases or decreases in dietary salt intake. It is proposed that the net effect of changes in dietary salt on sympathetic activity is determined by the balance between simultaneous and parallel sympathoinhibitory and sympathoexcitatory humoral mechanisms. A key element of the sympathoinhibitory mechanism is the chronic sympathoexcitatory effects of angiotensin II (ANG II). When salt intake increases, ANG II levels fall, and the sympathoexcitatory actions of ANG II are lost. Simultaneously, a sympathoexcitatory pathway is triggered, possibly via increases in osmolality which activate osmoreceptors or sodium receptors. In normal individuals, the sympathoinhibitory effects of increased salt predominate, sympathetic activity decreases, and arterial pressure remains normal despite salt and water retention. However, in subjects with salt‐sensitive hypertension, it appears that the sympathoexcitatory effects of salt predominate, possibly due to an inability to adequately suppress the levels or actions of ANG II. The net result, therefore, is an inappropriate increase in sympathetic activity during increased dietary salt which may contribute to the hypertensive process.

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“…discussion The renin-angiotensin system plays a key role in the adaptational events that allow mammals to maintain positive sodium balances when dietary sodium is restricted (Laragh & Sealey, 1973;Brunner & Gavras, 1980). In the present experiments, the control animals placed on the sodium-deficient regime gave the usual responses to sodium deprivation with increased plasma renin activities, increased peripheral aldosterone concentrations, reduced renal sodium excretion and overall urinary dilution (Spielman & Davis, 1974; Mosley, Hargreaves, Balment & Henderson, 1978;Hall, Guyton, Smith & Coleman, 1979;Tarjan, Spät, Balla & Szekely, 1980). These consequences of reduced dietary sodium were significantly modified by simultaneous treatment with captopril.…”

Section: Resultsmentioning

confidence: 65%

Influence of captopril on fluid and electrolyte balances and adrenocortical responses during sodium deprivation in the rat

McKeever¹,

Oliver²,

Henderson³

et al. 1983

Journal of Endocrinology

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An angiotensin I-converting enzyme inhibitor (captopril) was given by gastric lavage at a dose of 30 mg/kg body weight per day to Long-Evans rats for a 13-day period during which they received a sodium-deficient diet. This regime was preceded by a 3-day period during which measurements were made on the animals on a sodium-replete dietary intake. Control sodium-deprived rats showed increased plasma renin activities, increased peripheral aldosterone concentrations and reduced urinary sodium excretion; they maintained positive sodium balance and the zona glomerulosa of the adrenal cortex hypertrophied. Captopril-treated sodium-deprived rats failed to reduce urinary sodium excretion sufficiently and entered a period of marked and sustained negative sodium balance. Peripheral aldosterone concentrations after 12 days of sodium deprivation in the presence of captopril treatment were similar to those of sodium-replete rats. The adrenocortical zona glomerulosa of the captopril-treated rats did not increase in size and regressive changes were noted.

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Role of the renin-angiotensin system in the adaptation of aldosterone biosynthesis to sodium restriction in the rat

Cited by 14 publications

References 0 publications

Upregulation and intrarenal redistribution of heat shock proteins 90α and 90β by low-sodium diet in the rat

Upregulation and intrarenal redistribution of heat shock proteins 90α and 90β by low-sodium diet in the rat

The Interaction of Angiotensin II and Osmolality in the Generation of Sympathetic Tone during Changes in Dietary Salt Intake

Influence of captopril on fluid and electrolyte balances and adrenocortical responses during sodium deprivation in the rat

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