Kidney and Adrenocortical Hormones

Kleeman, Charles R.; Levi, J; Better, Ori S.

doi:10.1159/000180516

Cited by 42 publications

(17 citation statements)

References 64 publications

(148 reference statements)

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“…Moreover, these rats had significantly decreased urinary output during the entire experimental period (Fig. 1A), consistent with previous observations of impaired water excretion in response to glucocorticoid deficiency (23,24,29,41). In contrast, rats with aldosterone deficiency had significantly increased urinary output at the early stage after ADX (days 1-4, Fig.…”

Section: Glucocorticoid Deficiency and Mineralocorticoid Deficiency Isupporting

confidence: 91%

“…The observed decrease in urinary output is consistent with previous studies demonstrating that glucocorticoid deficiency is associated with an impaired water diuresis (19,23,29,41) and glucocorticoid treatment has been shown to restore this defect (29), partly by augmenting atrial natriuretic peptide (ANP) action (18). The impaired excretion of water by the kidney in glucocorticoid deficiency has been extensively investigated (1,16,19,24,29,41).…”

Section: Changes In Water Metabolism In Response To Glucocorticoid Desupporting

confidence: 88%

“…Adrenocortical hormones, glucocorticoid and mineralocorticoid, are importantly involved in the normal modulation of renal water excretion and regulation of ECF volume (23,29,37,41,42). Therefore, chronic adrenal insufficiency with depletion of adrenocortical hormones is associated with altered water and Na metabolism (40), e.g., an inability to excrete a water load in glucocorticoid deficiency (18,19,24) or increased urinary flow and natriuresis in aldosterone deficiency (44).…”

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confidence: 99%

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Regulation of collecting duct AQP3 expression: response to mineralocorticoid

Kwon

Nielsen

Masilamani

et al. 2002

American Journal of Physiology-Renal Physiology

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Adrenocortical steroid hormones are importantly involved in the regulation of extracellular fluid volume. The present study was aimed at examining whether aldosterone and/or glucocorticoid regulates the abundance of aquaporin-3 (AQP3), -2, and -1 in rat kidney. In protocol 1, rats were adrenalectomized, followed by aldosterone replacement, dexamethasone replacement, or combined aldosterone and dexamethasone replacement (rats had free access to water but received a fixed amount of food). Protocol 2 was identical to protocol 1, except that all groups received fixed daily food and water intake. In both protocols 1 and 2, aldosterone deficiency was associated with increased fractional Na excretion and severe hyperkalemia. Semiquantitative immunoblotting revealed that aldosterone deficiency was associated with a dramatic downregulation of AQP3 abundance. Consistent with this, immunocytochemistry and immunoelectron microscopy revealed a marked decrease in AQP3 labeling in the basolateral plasma membranes of collecting duct principal cells. In contrast, AQP1 and AQP2 abundance and distribution were unchanged. Glucocorticoid deficiency revealed no changes in AQP3, -2, or -1 abundance. In protocol 3, Na restriction (to increase endogenous aldosterone levels) or exogenous aldosterone infusion in either normal rats or vasopressin-deficient Brattleboro rats was associated with a major increase in AQP3 abundance. In protocol 4, aldosterone levels were clamped by infusion of aldosterone, while Na intake was altered from a low to a high level. Under these circumstances, there were no changes in AQP3 or AQP2 abundance, although the level of the thiazidesensitive Na-Cl cotransporter was decreased. In conclusion, the results uniformly demonstrate that aldosterone regulates AQP3 abundance independently of Na intake. In contrast, changes in glucocorticoid levels in these models do not influence AQP3 or AQP2 abundance. Therefore, in the collecting duct aldosterone may regulate, at least in part, AQP3 expression in addition to regulating Na and K transport.adrenalectomy; aquaporin; glucocorticoid; mineralocorticoid; vasopressin RENAL REGULATION OF WATER and Na reabsorption or excretion is critical to the regulation of extracellular fluid (ECF) volume. Adrenocortical hormones, glucocorticoid and mineralocorticoid, are importantly involved in the normal modulation of renal water excretion and regulation of ECF volume (23,29,37,41,42). Therefore, chronic adrenal insufficiency with depletion of adrenocortical hormones is associated with altered water and Na metabolism (40), e.g., an inability to excrete a water load in glucocorticoid deficiency (18,19,24) or increased urinary flow and natriuresis in aldosterone deficiency (44). Moreover, elevated vasopressin and ANG II levels secondary to the altered ECF volume status (29, 41) may also contribute to the change in water balance, e.g., an impairment of free water clearance and dilutional hyponatremia (43). However, there is little information available regarding the selective effect of glu...

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Section: Glucocorticoid Deficiency and Mineralocorticoid Deficiency Isupporting

confidence: 91%

Section: Changes In Water Metabolism In Response To Glucocorticoid Desupporting

confidence: 88%

mentioning

confidence: 99%

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Regulation of collecting duct AQP3 expression: response to mineralocorticoid

Kwon

Nielsen

Masilamani

et al. 2002

American Journal of Physiology-Renal Physiology

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“…However, as the decline in blood pressure and glomerular filtration was not apparent in animals in which only the posterior lobe ofthe pituitary had been removed (Balment, Brimble, Forsling, Kelly & Musabayane, 1986), it would appear to result from the loss of one or more of the anterior pituitary factors, or of the hormones whose secretion they regulate. There is indeed evidence that glomerular filtration is impaired if glucocorticoid secretion is reduced to low levels as a result of loss of pituitary corticotrophin (Cutler, Kleeman, Koplowitz, Maxwell & Dowling, 1962;Kleeman, Levi & Better, 1975), and it has been shown that administration of exogenous corticotrophin can partially restore arterial blood pressure and glomerular filtration in chronically hypophysectomized rats (Bauman, 1967;Bauman & Phillips, 1970).…”

Section: Discussionmentioning

confidence: 99%

The influence of neurohypophysial hormones on renal function in the acutely hypophysectomized rat.

Balment¹,

Brimble²,

Forsling³

et al. 1986

The Journal of Physiology

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1. Renal function and the effect of neurohypophysial hormone replacement was investigated in anaesthetized, acutely hypophysectomized, male rats. 2. Although urine production was only slightly lower over the 8 h post-operative study period in hypophysectomized rats, sodium excretion was greatly depressed reaching only 3.5 +/- 1.4 mumol/min compared with a peak of 13.2 +/- 1.0 mumol/min in intact animals. 3. In association with a decline in mean arterial blood pressure, glomerular filtration rate in hypophysectomized rats fell to 2.1 +/- 0.2 ml/min 8 h after operation by comparison with a mean rate in intact rats of 3.2 +/- 0.2 ml/min. 4. Plasma corticosterone levels were much lower in hypophysectomized (4 +/- 2 ng/ml) than in intact (36 +/- 4 ng/ml) rats, plasma aldosterone was reduced to a lesser extent (0.41 +/- 0.08 compared with 0.76 +/- 0.04 ng/ml). While oxytocin was not detectable in hypophysectomized rat plasma, trace levels of vasopressin (0.16 +/- 0.04 mu u./ml) were found. In intact unanaesthetized rats basal plasma levels of oxytocin were 0.32 +/- 0.13 mu u./ml and vasopressin were 0.85 +/- 0.19 mu u./ml. 5. Administration of oxytocin at 150 mu u./min, which produced plasma hormone levels (24.0 +/- 2.5 mu u./ml) greatly in excess of basal concentrations, increased renal sodium excretion but did not alter urine flow. Oxytocin administration at the lower rate of 15 mu u./min producing plasma hormone levels of 2.60 +/- 0.1 mu u./ml, did not alter renal sodium excretion. 6. Arginine vasopressin administered at 12 mu u./min induced plasma hormone levels of 1.54 +/- 0.09 mu u./ml and produced a large antidiuresis and small increase in the rate of sodium excretion. 7. The natriuretic response to vasopressin was potentiated by concurrent administration of oxytocin at 15 mu u./min. The peak sodium excretion of 5.8 +/- 1.0 mumol/min, however, remained well below that seen in intact rats. 8. It is concluded that, as restoration of posterior pituitary hormones at or above the physiological range only partially restored sodium excretion, the absence of anterior pituitary factors may also contribute directly or indirectly to the renal sodium retention of the hypophysectomized rat.

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“…As the kidney matures it becomes capable of increasing distal tubular sodium reabsorption to compensate for any increased distal tubular fluid delivery. (Pediatr Res 26: [6][7][8][9][10]1989) Abbreviations FRN,, fractional reabsorption of sodium FR,,i, fractional reabsorption of lithium uN,,v, uKV, UclV, Uc.V, renal excretion rate of sodium/ potassium/chloride/calcium may be responsible for neonatal hyponatremia. However, subsequent investigations have shown that a characteristic of this defect is decreased proximal tubule reabsorption of sodium (2) implying that renal insensitivity to aldosterone may be only partially responsible.…”

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confidence: 99%

Gestational Changes in Renal Responsiveness to Cortisol in the Ovine Fetus

1989

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ABSTRACT. The ontogenetic renal responsiveness to exogenous cortisol was examined in the chronically cannulated ovine fetus. The contribution of effects a t proximal and distal tubule of the kidney were studied also. Cortisol (81.5 pg/h) was infused into immature ovine fetuses (mean gestational age -113.9 days) on five occasions and increased blood cortisol from 0.8 f 0.5 to 21.3 + 6.2 nmol/ liter. This dose of cortisol produced a highly significant diuresis and natriuresis, in part due to an increase in GFR and in part due to a significant decrease in proximal tubular reabsorption of sodium. Cortisol (107.2 + 4.7 &h) was infused into mature fetuses (mean gestational age 133.4 days) and produced an increase in blood cortisol concentration from 11.4 + 5.6 to 33.7 2 6.8 nmol/liter. No natriuresis or diuresis was seen in the mature fetuses. Cortisol caused a significant depression of proximal tubular sodium reabsorption in mature fetuses, but this extra load was reabsorbed in the distal tubule in these fetuses. The inability of the premature or very low birth wt baby to maintain normal sodium balance on a standard salt intake may be due, at least in part, to a "fetal" renal response to the high plasma cortisol concentrations found in such babies. As the kidney matures it becomes capable of increasing distal tubular sodium reabsorption to compensate for any increased distal tubular fluid delivery. (Pediatr Res 26: 6-10, 1989) Abbreviations FRN,, fractional reabsorption of sodium FR,,i, fractional reabsorption of lithium uN,,v, uKV, UclV, Uc.V, renal excretion rate of sodium/ potassium/chloride/calcium may be responsible for neonatal hyponatremia. However, subsequent investigations have shown that a characteristic of this defect is decreased proximal tubule reabsorption of sodium (2) implying that renal insensitivity to aldosterone may be only partially responsible. The relative immaturity of renal function in very low birth wt and premature neonates seems to be important in the pathogenesis of hyponatremia. Premature neonates exhibit a greater natriuresis and a lower GFR in response to oral salt loading when compared to full-term neonates (5, 6). This is consistent with histopathologic studies that show that glomerular formation in the human infant is not complete until late in gestation (7), whereas tubular development is not complete until 1 y after birth (8).In mature mammals the presence of adrenal steroids is essential for normal renal function. A characteristic of adrenalectomized or hypophysectomized animals and patients with adrenal or pituitary insufficiency is a delayed diuresis following oral or parenteral water loading, accompanied by impaired sodium conservation and reduced GFR and renal blood flow. Administration of deoxycortisone acetate or aldosterone in the presence of normal sodium balance and extra-cellular volume has no effect on the delayed diuresis, whereas cortisol-like steroids correct this diuresis (9-1 1).Clinical investigations have reported that premature neonates have higher plasma co...

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Kidney and Adrenocortical Hormones

Cited by 42 publications

References 64 publications

Regulation of collecting duct AQP3 expression: response to mineralocorticoid

Regulation of collecting duct AQP3 expression: response to mineralocorticoid

The influence of neurohypophysial hormones on renal function in the acutely hypophysectomized rat.

Gestational Changes in Renal Responsiveness to Cortisol in the Ovine Fetus

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