Importance of sodium intake and mineralocorticoid hormone in the impaired water excretion in adrenal insufficiency

Ufferman, R. C.; Schrier, Robert W.

doi:10.1172/jci106965

Cited by 100 publications

(11 citation statements)

References 29 publications

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“…Analysis of the present results with previous studies from our laboratory in conscious adrenalectomized dogs (18) provides information about the separate effects of glucocorticoid and mineralocorticoid hormone. Mineralocorticoid deficiency in the presence of glucocorticoid replacement was shown previously to impair renal water excretion (18).…”

Section: Plasma Vasopressin In Glucocorticoid Deficiencymentioning

confidence: 51%

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Role of Plasma Vasopressin in Impaired Water Excretion of Glucocorticoid Deficiency

Boykin¹,

deTORRENTE²,

Erickson³

et al. 1978

J. Clin. Invest.

112

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A B S T R A C T In the present study, the effect of selective glucocorticoid deficiency on renal water excretion was investigated in conscious, trained, adrenalectomized dogs. The animals were studied before and after a water load while on replacement therapy of desoxycorticosterone acetate, 5 mg/day, and dexamethasone, 0.8 mg/day (group I), and while off dexamethasone for 5-9 days (group II). Before the water load the weight, inulin space, cardiac output, blood pressure, glomerular filtration rate, renal blood flow, plasma osmolality, and plasma antidiuretic hormone measured by radioimmunoassay were similar in both groups I and II. However, after a 40 ml/kg water load a marked impairment in renal water excretion in the glucocorticoid deficient dogs became apparent. Maximal free water clearance was -0.046±0.16 vs. 6.51±0.72 ml/min (P < 0.001) and minimal urinary osmolality was 425±56 vs. 82±3.5 mosmol/kg H20 (P < 0.001) in group II as compared to group I. Plasma antidiuretic hormone was maximally suppressed during the water load in group I to 0.34±0.08 pg/ml but remained elevated at 9.18±1.79 pg/ml (P <0.005) in group II. This nonsuppressibility of plasma antidiuretic hormone during water loading in group II was associated with a significant tachycardia of 145±6 vs. 87±6 beats/min (P < 0.001) in group I and a significantly lower stroke volume of 27±0 vs. 59±0.5 ml/beat (P < 0.001). In conclusion, our results implicate a persistent secretion of antidiuretic hormone as an important factor in the impaired water excretion of glucocorticoid deficiency. A deleterious effect of glucocorticoid deficiency on cardiac function was observed and this hemodynamic alteration could be involved in initiating a nonosmolar, baroreceptormediated release of vasopressin.

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Section: Plasma Vasopressin In Glucocorticoid Deficiencymentioning

confidence: 51%

“…In previous studies from our laboratory mineralocorticoid replacement alone was demonstrated to correct totally the impaired water excretion in conscious adrenalectomized dogs. The duration of withdrawal of glucocorticoid hormone replacement from these animals, however, ranged from 50 to 100 h (18).…”

Section: Introductionmentioning

confidence: 99%

Role of Plasma Vasopressin in Impaired Water Excretion of Glucocorticoid Deficiency

Boykin¹,

deTORRENTE²,

Erickson³

et al. 1978

J. Clin. Invest.

112

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“…The decreases in serum cortisol and plasma aldosterone are involved in the Na-losing state. Also, the patients with isolated ACTH deficiency became inactive and had a poor appetite, and Na intake was probably reduced [17]. These Na-losing states are probably related to hypovolemia in our patients.…”

Section: Laboratory Findingsmentioning

confidence: 59%

Role of Antidiuretic Hormone in Hyponatremia in Patients with Isolated Adrenocorticotropic Hormone Deficiency.

Ishikawa¹,

Fujisawa²,

Tsuboi³

et al. 1991

Endocrinol Japon

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Abstract.We found symptomatic hyponatremia in four elderly patients in which serum sodium (Na) levels ranged from 101 to 122 mEq/l. All 4 patients had low levels of plasma adrenocorticotropic hormone (ACTH), serum cortisol, and urinary excretion of 17-OHCS, and poor responses of ACTH to exogenous insulin and antidiuretic hormone (ADH). Other pituitary hormones were all normal. They were therefore diagnosed as having isolated ACTH deficiency. Plasma ADH was relatively high despite hypoosmolality which was associated with the hyponatremia. Water loading test revealed impaired water excretion and poor suppression of plasma ADH. Replacement with 20-30 mg hydrocortisone completely restored the serum Na level and restored the plasma ADH level to the normal range in all 4 patients. Other factors such as decreased glomerular filtration, enhanced urinary Na loss and decreased Na intake were also included. These results indicate that there is marked hyponatremia and that in the presence of hypoosmolality the sustained secretion of ADH is the key factor in causing the impaired water excretion and hyponatremia in isolated ACTH deficiency.

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“…The mineralocorticoid deficiency also is responsible for the sodium chloride wasting and extracellular fluid volume depletion in primary adrenal insufficiency. Selective mineralocorticoid deficiency has been studied in adrenalectomized animals that received replacement glucocorticoid hormone (31)(32)(33). With isolated mineralocorticoid hormone deficiency and hyponatremia, plasma AVP concentrations were not suppressed and collecting duct AQP2 and 3 expressions were upregulated.…”

Section: Addison's Disease and Hypopituitarismmentioning

confidence: 99%

Body Water Homeostasis

Schrier¹

2006

Journal of the American Society of Nephrology

172

107

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T he discovery of the aquaporin-1 (AQP1) water channel by Agre and colleagues (1,2), which led to the Nobel Prize in 2003, has revolutionized the understanding of body fluid water regulation by the kidney. Moreover, the identification of other water channels in the kidney, namely AQP2, 3, and 4, along with urea and ion transporters, has allowed a much improved understanding of urinary dilution and concentration in health and disease at the cellular and molecular levels (3-8).The AQP have provided a pathway for water movement across cellular membranes that could not be explained by simple diffusion through the lipid bilayers of cell membranes. AQP1 has been found to be expressed constitutively on both the apical and the basolateral membranes of the proximal tubule and descending limb of Henle's loop. This water channel is not under control of vasopressin but is important in urinary concentration. Water efflux through these channels in the descending limb is an important factor in the countercurrent concentrating mechanism, and diminished maximal urinary osmolality has been shown in AQP1 knockout mice (9) and humans without the AQP1 gene (10).AQP2, 3, and 4 are expressed in the cortical and medullary collecting duct ( Figure 1) (11). AQP2 is found exclusively in the principal cells of the collecting tubule and collecting duct and is known to be regulated by arginine vasopressin (AVP). AQP3 and 4 are located on the basolateral membrane of the principal cells in the collecting duct. AQP3 knockout mice exhibit substantial polyuria secondary to vasopressin-resistant nephrogenic diabetes insipidus (NDI) (12). AQP3 is regulated by AVP. AQP4 predominates on the basolateral membrane of the inner medulla and is not regulated by AVP. AQP4 knockout mice also exhibit an NDI that is less severe than that observed in the AQP3 knockout mice (13). Whereas AQP3 and AQP4 constitute the exit channels for water movement across the basolateral membrane of the collecting duct, AQP2 is the water channel for water reabsorption across the apical membrane of the principal cells of the collecting duct. These transgenic mouse models of AQP deletion/mutation are of importance not only for kidney function but also for other epithelia (14).AVP regulates AQP2 in both an acute (short term) (15) and chronic (long term) manner (16,17). The short-term regulation by AVP involves trafficking of vesicles that contain AQP2 to the apical membrane with resultant increased water permeability. Suppression of plasma AVP reverses this exocytosis of AQP2, and the vesicles are retrieved from the membrane (endocytosis) into the cytoplasm. Both the short-and long-term regulation of AQP2 by AVP is initiated by activation of the V2 receptor on the basolateral membrane of the collecting duct. The binding of AVP to the V2 receptor, which is coupled to a guanine-nucleotide-binding protein Gs, results in activation of adenylyl cyclase. This results in an increase in intracellular cAMP concentration that mediates the activation of protein kinase A (PKA). Activated PKA p...

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Importance of sodium intake and mineralocorticoid hormone in the impaired water excretion in adrenal insufficiency

Cited by 100 publications

References 29 publications

Role of Plasma Vasopressin in Impaired Water Excretion of Glucocorticoid Deficiency

Role of Plasma Vasopressin in Impaired Water Excretion of Glucocorticoid Deficiency

Role of Antidiuretic Hormone in Hyponatremia in Patients with Isolated Adrenocorticotropic Hormone Deficiency.

Body Water Homeostasis

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