Studies on Alcohol Diuresis. Iii. The Response to Ethyl Alcohol in Certain Disease States Characterized by Impaired Water Tolerance 1

Lamdin, Ezra; Rubini, Milton E.; Epstein, Franklin H.

doi:10.1172/jci103289

Cited by 39 publications

(6 citation statements)

References 16 publications

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“…If, as available data suggests, compound F like steroids does not alter metabolism of antidiuretic hormone (4,7,(9)(10)(11)(12)(13), the present studies lend further support to the concept that these steroids improve water diuresis by inhibiting the back diffusion of water in diluting segments of the nephron; a permissive action.…”

Section: A Response To Water Loading: Althoughsupporting

confidence: 75%

“…This defect can only be corrected by administration of hydrocortisone-like steroids ( 3 -6 ) , probably by direct effect on kidney rather than by extra-renal mechanisms (4,7,(9)(10)(11)(12) . Hydrocortisone increases glomerular filtration, renal blood flow and enhances tubular reabsorption of sodium in the adrenal and pituitary insufficient subject (7)(8)(9)(10)(11)(12). However, our previous studies indicate that marked improvement in water diuresis caused by compound F cannot be explained solely by its effects on renal hemodynamics or solute excretion ( 7).…”

mentioning

confidence: 99%

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Acute Effect of 6 Methyl Prednisolone (Medrol(R)) on Impaired Water Excretion of Adrenal and Pituitary Insufficiency.

Koplowitz

Maxwell

1959

Experimental Biology and Medicine

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An impaired diuretic response to water is a characteristic abnormality of patient or animal with adrenal or pituitary insufficiency (1-6). This defect can only be corrected by administration of hydrocortisone-like steroids ( 3 -6 ) , probably by direct effect on kidney rather than by extra-renal mechanisms (4,7,(9)(10)(11)(12) . Hydrocortisone increases glomerular filtration, renal blood flow and enhances tubular reabsorption of sodium in the adrenal and pituitary insufficient subject (7-12). However, our previous studies indicate that marked improvement in water diuresis caused by compound F cannot be explained solely by its effects on renal hemodynamics or solute excretion( 7). It seemed therefore of interest to note the effect of MedroP (6 methyl prednisolone) on impaired diuresis of adrenal and pituitary insufficiency. This potent adrenal cortical analogue does not enhance sodium reabsorption or alter renal hemodynamics in normal subjects (13). Materials and methods.Six experiments were performed in 6 male patients: 4 with anterior pituitary insufficiency (secondary adrenal insufficiency) and 2 with primary adrenal insufficiency. Hydrocortisone replacement therapy was withdrawn from all patients for at least 1 week prior to experiments. Subjects with primary adrenal insufficiency were maintained on 100 pg of 9-alpha fluoro-hydrocortisone daily. Experiments were performed in the morning post-prandially, with subjects recumbent. An initial urine specimen was obtained for osmolality, after which an oral water load of 1000 cc was given; this positive water balance was maintained for duration of experiment by infusion of 2.5% glucose in water at a rate equal to urine flow. Collection periods were 20 to 30 minutes, and urine samples collected by spontaneous voiding or by in-*Supported by grants from the Upjohn Co. and Arie Crown Fund. dwelling catheters. When urine volume was below 2 cc/minute, air "wash outs" were also utilized. Samples of venous blood were obtained at midpoint of each period through an indwelling needle. Control collections were begun about 45 minutes after priming dose of inulin and para amino-hippurate and constant sustaining infusion had been started. After at least 3 control periods of maximally sustained urinary flow had been obtained (approximately 2% hours after initiating the water load), 5-20 mg of MedrolB were administered into infusion tubing for 30 minutes. Urinary collections were continued for additional 3 to 5 hours. Experiments ranged from 5 5 to 8 hours in duration. Analysis of serum and urine for sodium, potassium, chloride, indin, PAH, creatinine, and freezing point depression (osmolality : milliosmols/kg of H20) were made utilizing methods previously reported ( 14,15). Characteristics of water diuresis were evaluated in each case by maximal urinary flow, minimal urinary osmolality and magniltude of free water clearance CHzO. t Since the experiments were too rigorous to permit control water loading studies without drug administration on each subject, urine volumes were measured...

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Section: A Response To Water Loading: Althoughsupporting

confidence: 75%

mentioning

confidence: 99%

Acute Effect of 6 Methyl Prednisolone (Medrol(R)) on Impaired Water Excretion of Adrenal and Pituitary Insufficiency.

Koplowitz

Maxwell

1959

Experimental Biology and Medicine

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“…), does not modify the response of the neurohypophyseal system to osmotic and nonosmotic stimuli and does not antagonize the peripheral action of ADH (34). Furthermore, earlier investigations have shown 1) that alcohol, a strong inhibitor of the neurohypophyseal system, does not initiate a water diuresis in adrenal insufficiency unless hydrocortisone is previously given (35,36), and 2) that there is no increased sensitivity to or delayed inactivation of ADH in patients with adrenal and pituitary insufficiency (6). These observations suggest that an extrarenal mechanism altering the metabolism of ADH is not responsible for the impaired water excretion in these states.…”

Section: Discussionmentioning

confidence: 94%

Mechanisms of Impaired Water Excretion in Adrenal and Pituitary Insufficiency. I. The Role of Altered Glomerular Filtration Rate and Solute Excretion12

Maxwell¹,

Rockney²

1958

J. Clin. Invest.

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The inability to excrete an oral or parenteral load of water in a normal manner is a characteristic of the adrenalectomized or hypophysectomized animal and of the patient with adrenal or pituitary insufficiency ( 1-9). This defect persists in the presence of a normal salt balance, extracellular volume, and an adequate supply of salt-retaining hormone, desoxycorticosterone acetate (DCA) or aldosterone (4,7,8,10,11), but it can usually be corrected by the administration of hydrocortisone-like steroids (3,4,7,9).The basic mechanisms responsible for impaired water tolerance in these diseases have not been adequately clarified, nor have the processes by which hydrocortisone causes a normal water diuresis to occur.Gaunt, Birnie and Eversole (8) and others (7, 12) have suggested that a homeostatic "balance" exists between the antidiuretic hormone (ADH) of the neurohypophysis and the 11, 17 hydroxylated steroids of the adrenal cortex. They suggest that in the absence of these steroids, a relative or absolute excess of ADH exists, preventing a normal water diuresis. To prove this hypothesis, a sustained level of secretion of ADH should be demonstrated after the adrenal or anterior pituitary deficient animal has been water loaded, a procedure which ordinarily inhibits ADH secretion. To date, no such sustained activity has been observed using a generally acceptable and specific assay technique (6,13,14). Furthermore, the patient with adrenal or pituitary insufficiency normally inactivates and is not hypersensitive to exogenous antidiuretic hormone (Pitressin®) (6). Recent studies have stressed the importance of nonhormonal factors in determining the characteristics of water diuresis in normal subjects. The rate of glomerular filtration and solute excretion, and the distribution of the reabsorbed solutes between the proximal and distal tubules can profoundly alter the diuretic response to water in the absence of circulating ADH (15-21). Reduced glomerular filtration and renal blood flow are usually present in subjects with pituitary and adrenal insufficiency. In the latter, and occasionally in the former group, tubular reabsorption of sodium is impaired. Welt (22) postulated that the impaired water diuresis of these states is related primarily to alterations in the nonhormonal factors rather than to any disturbance in the secretion, metabolism, or action of ADH. If this theory is correct, it should be possible, while these subjects are under the influence of a sustained water load, to improve considerably their response to water loading by techniques which increase glomerular filtration rate and alter the distribution of solute (sodium) reabsorption between the proximal and distal tubule.This approach formed the basis of the present study. Aminophyllin was used to increase glomerular filtration acutely and alter the tubular reabsorption of solute. Its effect was compared in the same subject with the subsequent administration of hydrocortisone. The results indicate that the marked improvement in the execretion of water which...

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“…Previous clinical studies have demonstrated a markedly imparied water diuresis after water loads in both congestive heart failure (2) and decompensated hepatic cirrhosis (14). This finding PM: 12 hr later urine samples were collected each hour for is thought to reflect increased reabsorption of sodium in the osmolality until values changed by less than 30 mOsmjkg H 2 0 proximal portion of the nephron (18).…”

Section: Speculationmentioning

confidence: 87%

A Study of the Renal Handling of Water in Lipoid Nephrosis

et al. 1976

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Studies on Alcohol Diuresis. Iii. The Response to Ethyl Alcohol in Certain Disease States Characterized by Impaired Water Tolerance 1

Cited by 39 publications

References 16 publications

Acute Effect of 6 Methyl Prednisolone (Medrol(R)) on Impaired Water Excretion of Adrenal and Pituitary Insufficiency.

Acute Effect of 6 Methyl Prednisolone (Medrol(R)) on Impaired Water Excretion of Adrenal and Pituitary Insufficiency.

Mechanisms of Impaired Water Excretion in Adrenal and Pituitary Insufficiency. I. The Role of Altered Glomerular Filtration Rate and Solute Excretion12

A Study of the Renal Handling of Water in Lipoid Nephrosis

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