Excretion of aldosterone in inappropriate secretion of antidiuretic hormone following head trauma

Knöchel, James P.; Osborn, James; Cooper, Everett B.

doi:10.1016/0026-0495(65)90055-7

Cited by 34 publications

(9 citation statements)

References 23 publications

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“…Second, hyponatremia is considered a pathophysiological state, and the classic stimuli are generally considered to be the major contributors to aldosterone stimulation under normal physiological conditions. Third, there appears to be a delay in the rise in aldosterone relative to the development of hyponatremia, making it unclear what the stimulus for secretion truly is (22). As early as 1965, Knochel and associates (22) reported a delayed rise in aldosterone excretion in a patient with SIADH administered a water load.…”

Section: Discussionmentioning

confidence: 96%

“…Third, there appears to be a delay in the rise in aldosterone relative to the development of hyponatremia, making it unclear what the stimulus for secretion truly is (22). As early as 1965, Knochel and associates (22) reported a delayed rise in aldosterone excretion in a patient with SIADH administered a water load. We speculate, as do others (22), that the "delay" in the appearance of hyperaldosteronism relative to the rapid development of hyponatremia may be the result of the competition between factors that decrease aldosterone, i.e., volume expansion, and factors that increase it, i.e., hyponatremia.…”

Section: Discussionmentioning

confidence: 96%

“…Several reports (1,6,7,22,23,30), going back decades, have reported evidence of increased aldosterone activity, i.e., plasma levels, urine excretion, and urine K ϩ -to-Na ϩ ratios in hyponatremia. These results were surprising, because SIADH is often associated with volume expansion, which is known to decrease activation of the renin-angiotensin system, thereby reducing ANG II stimulation of adrenal aldosterone secretion.…”

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confidence: 98%

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Increased blood pressure, aldosterone activity, and regional differences in renal ENaC protein during vasopressin escape

Song

Khan

et al. 2004

American Journal of Physiology-Renal Physiology

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The syndrome of inappropriate antidiuretic hormone (SIADH) is associated with water retention and hyponatremia. The kidney adapts via a transient natriuresis and persistent diuresis, i.e., vasopressin escape. Previously, we showed an increase in the whole kidney abundance of aldosterone-sensitive proteins, the alpha- and gamma (70-kDa-band)-subunits of the epithelial Na(+) channel (ENaC), and the thiazide-sensitive Na-Cl cotransporter (NCC) in our rat model of SIADH. Here we examine mean arterial pressure via radiotelemetry, aldosterone activity, and cortical vs. medullary ENaC subunit and 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD-2) protein abundances in escape. Eighteen male Sprague-Dawley rats (300 g) were sham operated (n = 6) or infused with desmopressin (dDAVP; n = 12, a V(2) receptor-selective analog of AVP). After 4 days, one-half of the rats receiving dDAVP were switched to a liquid diet, i.e., water loaded (WL) for 5-7 additional days. The WL rats had a sustained increase in urine volume and blood pressure (122 vs. 104 mmHg, P < 0.03, at 7 days). Urine and plasma aldosterone levels were increased in the WL group to 844 and 1,658% of the dDAVP group, respectively. NCC and alpha- and gamma-ENaC (70-kDa band) were increased significantly in the WL group (relative to dDAVP), only in the cortex. Beta- and gamma-ENaC (85-kDa band) were increased significantly by dDAVP in cortex and medulla relative to control. 11beta-HSD-2 was increased by dDAVP in the cortex and not significantly affected by water loading. These changes may serve to attenuate Na(+) losses and ameliorate hyponatremia in vasopressin escape.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 96%

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confidence: 98%

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Increased blood pressure, aldosterone activity, and regional differences in renal ENaC protein during vasopressin escape

Song

Khan

et al. 2004

American Journal of Physiology-Renal Physiology

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“…On the basis of the present observations, it would seem reasonable to suggest that a rise in aldosterone secretion induced by hyponatremia is responsible for the protection of acid-base equilibrium. Whether this explanation is, in fact, correct remains to be determined; elevated levels of aldosterone have been noted in some patients with this syndrome (15)(16)(17)(18)(19), but such increases have not been found consistently (20)(21)(22)(23). It thus seems clear that a systematic study of aldosterone secretion in these patients will be necessary to clarify the interplay between tonicity, aldosterone, and acid-base equilibrium.…”

Section: Resultsmentioning

confidence: 99%

The critical role of the adrenal gland in the renal regulation of acid-base equilibrium during chronic hypotonic expansion. Evidence that chronic hyponatremia is a potent stimulus to aldosterone secretion.

Cohen¹,

Hulter²,

Smithline³

et al. 1976

J. Clin. Invest.

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A B S T R A C T Recent studies have shown that chronic hypotonic volume expansion (HVE) induced by administration of vasopressin and water stimulates distal hydrogen ion secretion and thereby (a) permits dogs with HCl-acidosis to restore acid-base equilibrium to normal despite continued acid feeding and (b) permits normal dogs to conserve filtered bicarbonate quantitatively despite the natriuresis induced by water retention.To examine whether these effects of chronic HVE are mediated by augmented mineralocorticoid secretion, urinary and plasma aldosterone levels were monitored during prolonged administration of vasopressin. In HCl-fed animals, the HVE-induced rise in plasma [HCO3] (from 13.8 to 21.3 meq/liter) was associated with a rise in aldosterone excretion from 0.45 to 0.88 ,ug/day (P < 0.02). In normal animals, in which plasma [HCO3] remained stable during HVE (21.9 vs. 20.0 meq/liter), aldosterone excretion rose from 0.51 to 2.28 ug/day (P < 0.02) and plasma aldosterone concentration rose from 8.1 to 39.8 ng/100 ml (P < 0.01).Vasopressin and water were also administered to adrenalectomized animals maintained on glucocorticoids and a slightly subphysiologic replacement schedule of mineralocorticoids. In the HCl-fed adrenal- 15.0 meq/liter). In the non-HCl-fed adrenalectomized group, plasma [HCO3], rather than remaining stable, fell significantly (20.3 vs. 16.5 meq/liter, P < 0.1).Two conclusions can be drawn from this study: (a) the well-known inhibitory effect of volume expansion on aldosterone secretion can be ove-rridden by a potent stimulatory effect on the adrenal produced by severe chronic hypotonicity, and (b) the response of plasma [HCO3] observed during severe chronic HVE is mediated by augmented mineralocoiticoid secretion. These findings, furthermore, offer a possible explanation for the puzzling observation that plasma [HCO3] in patients with the syndrome of inappropriate antidiuretic hormone secretion is maintainied at normal levels even in the face of severe hyponatremiiia.

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“…In previously reported cases of SIADH, levels of aldo sterone were low [Ivy and Minn, 1961;Thorn and Transbol, 1963], normal [Knöchel et al, 1965;Clift et al, 1966;Michelakis and Horton, 1970], or elevated [Heinemann and Laragh, 1966;Fichman undßethune, 1968], ln experiments with dogs, chronic hypotonic expansion of body fluids produced a marked increment in aldosterone excretion [Cohen et al, 1976]. One explanation for the difference is the degree of hyponatremia.…”

Section: Discussionmentioning

confidence: 99%

Increased Urinary Kallikrein-Like Activity in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Tomita

Shiigai

Shichiri

et al. 1983

Nephron

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The role of the kallikrein system in the natriuresis of SIADH was studied in 3 patients. Following free water intake, serum Na decreased. Urinary Na excretion, urinary aldosterone excretion and urinary kallikrein-like activity (Uĸ_aV) increased. Significant relationships were observed between Uĸ_aV and urinary aldosterone excretion during the study. Further, there were significant relationships between serum Na and UĸaV, and between uric acid clearance and Uĸ_aV. In 1 patient, who was observed for a longer period, a significant relationship was observed between Na clearance and Uĸ_aV. We conclude that Uĸ_aV is increased during hyponatremia in SIADH by volume expansion. This increase in U_KaV may play a role in the natriuresis in SIADH.

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Excretion of aldosterone in inappropriate secretion of antidiuretic hormone following head trauma

Cited by 34 publications

References 23 publications

Increased blood pressure, aldosterone activity, and regional differences in renal ENaC protein during vasopressin escape

Increased blood pressure, aldosterone activity, and regional differences in renal ENaC protein during vasopressin escape

The critical role of the adrenal gland in the renal regulation of acid-base equilibrium during chronic hypotonic expansion. Evidence that chronic hyponatremia is a potent stimulus to aldosterone secretion.

Increased Urinary Kallikrein-Like Activity in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

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