Different effects of three aldosterone treatments on plasma aldosterone and salt intake

Tordoff, Michael G.; Hughes, Rebecca L.; Pilchak, Diane M.

doi:10.1016/0031-9384(93)90054-j

Cited by 11 publications

(6 citation statements)

References 20 publications

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“…Changes in UNaE excretion were also related to changes in LV geometry and diastolic filling properties, but these relationships did not persist when changes in LVMI were included in the multivariate model, indicating that UNaE is primarily associated with the increase in LV mass. Animal 35 and human 14 studies suggested that salt appetite may be stimulated by aldosterone levels with a mechanism that is likely related to the action of aldosterone on the brain. Therefore, persistence of elevated plasma aldosterone in patients treated with MRA (Table 2) could possibly account for lesser reduction in UNaE than adrenalectomy by increasing salt appetite.…”

Section: Discussionmentioning

confidence: 99%

Dietary Salt Intake Is a Determinant of Cardiac Changes After Treatment of Primary Aldosteronism

et al. 2016

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Primary aldosteronism is associated with increased left ventricular (LV) mass independently of blood pressure. Previous studies suggest that elevated aldosterone causes cardiac damage only in the presence of an inappropriate salt status. We examined the relevance of dietary salt intake on cardiac changes in patients with primary aldosteronism before and after treatment. Sixty-five patients with tumoral or idiopathic primary aldosteronism were recruited at a University medical center and followed after either surgical (n=30) or medical (n=35) treatment. At baseline and 1 year after treatment, cardiac morphology and functional variables were measured by echocardiography together with duplicate 24-hour urinary sodium collections. At baseline, LV mass index was associated with urinary sodium excretion and plasma aldosterone levels. During follow-up, blood pressure (from 167/102–135/83 mm Hg; P <0.001) and LV mass index (from 50.5±13.0–44.4±8.9 g/m 2.7 ; P <0.001) decreased significantly with nonsignificant changes in LV geometry and functional properties. At the end of follow-up, percentage decrease in LV mass index was significantly greater in patients who had >10% reduction in urinary sodium excretion (15.0±12.5%) than in the remaining patients (5.5±9.3%; P <0.001). Changes in LV mass index induced by both surgical and medical treatment were directly and independently correlated with changes in blood pressure (β=0.419; P =0.009) and urinary sodium excretion (β=0.334; P =0.012) observed at follow-up. These findings strongly support the hypothesis that dietary salt intake has a crucial role in aldosterone-related LV changes and could contribute to cardiac damage in patients with primary aldosteronism.

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Section: Discussionmentioning

confidence: 99%

Dietary Salt Intake Is a Determinant of Cardiac Changes After Treatment of Primary Aldosteronism

et al. 2016

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“…That this change in ingestive behaviour occurred specifically in response to sodium deficiency was confirmed by the demonstration that saline intake returned to normal when functional adrenal tissue was transplanted back into adrenalectomized rats (Richter & Eckert, 1938). Likewise, their increased saline intake vanished when sodium conservation was re‐instated using replacement‐dose mineralocorticoid injections (Wolf, 1965; Fregly & Waters, 1966), but promptly reappeared when hormone replacement was withdrawn (McEwen et al 1986; Tordoff et al 1993).…”

Section: What Is Sodium Appetite and Why Is It Important?mentioning

confidence: 99%

“…Although Richter's original experiments with adrenalectomy‐induced sodium appetite showed that this hormone is not necessary for sodium appetite, he subsequently discovered that treatment with high‐dose adrenal mineralocorticoids stimulated the ingestion of large volumes of saline, even in control animals (Rice & Richter, 1943). In low doses that merely restore baseline renal sodium conservation, the administration of an adrenal mineralocorticosteroid (aldosterone or others, such as deoxycorticosterone) reduces sodium appetite in an adrenalectomized animal (Wolf, 1965; Fregly & Waters, 1966; McEwen et al 1986; Tordoff et al 1993). Higher doses, however, robustly stimulate the ingestion of large amounts of saline in both adrenalectomized and adrenal‐intact rats (Wolf, 1965; Fregly & Waters, 1966).…”

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confidence: 99%

Central regulation of sodium appetite

Geerling

Loewy

2008

Experimental Physiology

237

197

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Sodium appetite, the behavioural drive to ingest salt, is stimulated by prolonged physiological sodium deficiency in many animal species. The same neural mechanisms that are responsible for sodium appetite in laboratory animals may influence human behaviour as well, with particular relevance to the dietary salt intake of patients with diseases such as heart failure, renal failure, liver failure and salt-sensitive hypertension. Since the original experimental work of Curt Richter in the 1930s, much has been learned about the regulation of salt-ingestive behaviour. Here, we review data from physiology, pharmacology, neuroanatomy and neurobehavioural investigations into the stimulatory and inhibitory signals that regulate sodium appetite. A rudimentary framework is proposed for the brain circuits that integrate peripheral information representing the need for sodium with neural signals for the gustatory detection of salt in order to drive a motivated ingestive response. Based on this model, areas of remaining uncertainty are highlighted where future information would allow a more detailed understanding of the neural circuitry responsible for sodium appetite.

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“…Substituting low doses of mineralocorticoids in these rats reduced renal salt excretion and saline intake [38, 53-55]; aldosterone levels around 85 pg/ml, which is well within the physiological range, resulted in the lowest saline intake [54]. Higher mineralocorticoid dosis increased saline intake in adrenalectomized rats [38, 55].…”

Section: Introductionmentioning

confidence: 99%

Mineralocorticoid-Induced Sodium Appetite and Renal Salt Retention: Evidence for Common Signaling and Effector Mechanisms

Fu¹,

Vallon²

2014

Nephron Physiol

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An increase in renal sodium chloride (salt) retention and an increase in sodium appetite are the body's responses to salt restriction or depletion in order to restore salt balance. Renal salt retention and increased sodium appetite can also be maladaptive and sustain the pathophysiology in conditions like salt-sensitive hypertension and chronic heart failure. Here we review the central role of the mineralocorticoid aldosterone in both the increase in renal salt reabsorption and sodium appetite. We discuss the working hypothesis that aldosterone activates similar signaling and effector mechanisms in the kidney and brain, including the mineralocorticoid receptor, the serum- and glucocorticoid-induced kinase SGK1, the ubiquitin ligase NEDD4-2, and the epithelial sodium channel ENaC. The latter also mediates the gustatory salt sensing in the tongue, which is required for the manifestation of increased salt intake. Effects of aldosterone on both the brain and kidney synergize with the effects of angiotensin II. Thus, mineralocorticoids appear to induce similar molecular pathways in the kidney, brain, and possibly tongue, which could provide opportunities for more effective therapeutic interventions. Inhibition of renal salt reabsorption is compensated by stimulation of salt appetite and vice versa; targeting both mechanisms should be more effective. Inhibiting the arousal to consume salty food may improve a patient's compliance to reducing salt intake. While a better understanding of the molecular mechanisms is needed and will provide new therapeutic options, current pharmacological interventions that target both salt retention and sodium appetite include mineralocorticoid receptor antagonists and potentially inhibitors of angiotensin II and ENaC.

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Different effects of three aldosterone treatments on plasma aldosterone and salt intake

Cited by 11 publications

References 20 publications

Dietary Salt Intake Is a Determinant of Cardiac Changes After Treatment of Primary Aldosteronism

Dietary Salt Intake Is a Determinant of Cardiac Changes After Treatment of Primary Aldosteronism

Central regulation of sodium appetite

Mineralocorticoid-Induced Sodium Appetite and Renal Salt Retention: Evidence for Common Signaling and Effector Mechanisms

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