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Biomedical subjects

F C Bartter

Publications and source records attributed to F C Bartter.

At least 37 records · Page 2Linked to original sources
PubMed1981

Acute effects of dietary protein on calcium metabolism in patients with osteoporosis.

Five untreated osteoporotic patients were studied in a metabolic unit for 30 days while receiving control (0.8 gm/kg) and high (2.0 gm/kg) protein diets of purified proteins. The high protein diet increased urinary calcium and produced a negative calcium balance without causing significant change in calcium absorption, serum chemical values, or urinary sodium and potassium. Variable effects of calcium and/or estrogens were found on the negative balance. Hence, increased dietary protein acutely causes a negative calcium balance in osteoporotic patients and may contribute to bone loss in this disease.

Calcium↗
PubMed1981

Overproduction of sodium-retaining steroids by the zona glomerulosa is adrenocorticotropin-dependent and mediates hypertension in dexamethasone-suppressible aldosteronism.

Dexamethasone suppressed urinary aldosterone to less than 1.5 micrograms/day in 1-2 days and lowered blood pressure in a woman and in her 2 1/2-yr-old daughter, both of whom have hypertension and hyporeninemia and are members of a kindred with dexamethasone-suppressible aldosteronism. ACTH given for 7 days produced a sustained increase in aldosterone production and a rise in blood pressure in both patients. The abnormal suppression with dexamethasone and further stimulation with ACTH indicate that the aldosteronism is ACTH-dependent in this disorder. The cause of the ACTH-dependence of aldosterone production in this disorder is unknown but may represent continued stimulation rather than the usual (secondary) inhibition by ACTH of 11-hydroxylation and 18-hydroxylation in zone glomerulosa cells. Blood pressure was normal during treatment with spironolactone and during pregnancy, when the action of aldosterone and other similar steroids was presumably blocked by an increased production of progesterone; this suggests that the hypertension is dependent upon sodium-retaining steroids such as aldosterone. Aminoglutethimide given during treatment with ACTH decreased urinary aldosterone and blood pressure and increased PRA, with minimal effects on plasma cortisol or urinary 17-hydroxycorticosteroids. These results provide additional evidence that aldosterone, acting alone or in conjunction with other steroids synthesized by the zona glomerulosa, mediates the hypertension and hyporeninemia of dexamethasone-suppressible aldosteronism.

Adrenal Cortex↗
PubMed1981

Resolution of longstanding protein-losing enteropathy in a patient with intestinal lymphangiectasia after treatment for malignant lymphoma.

In 1956 we evaluated a patient who had a debilitating disease of a 2 yr duration, characterized by recurrent vomiting, diarrhea, cachexia, massive edema, hypoproteinemia, and dilated intestinal lymphatics. During our initial evaluation of this patient, we observed that 42% of her circulating protein pool was lost into her gastrointestinal tract daily, whereas normal gastrointesinal loss of protein does not exceed 1.6%. Her disease appeared to represent a classic example of intestinal lymphangiectasia. She was treated symptomatically for 13 yr with essentially no change. In 1969 the patient developed a stage IV diffuse, undifferentiated (non-Burkitt's) malignant lymphoma. Using immunoperoxidase staining, the neoplastic cells were found to contain cytoplasmic IgMKappa, suggesting that the lymphoma had a monoclonal B-cell origin. She was successfully treated with cyclophosphamide, vincristine, and prednisone. Shortly after the initiation of this systemic combination chemotherapy, her serum protein concentration returned to normal, her edema resolved, and she was cured of gastrointestinal symptoms. Moreover, repeat studies revealed that her protein loss had fallen to only 2%. The simultaneous cure of both the intestinal lymphangiectasia and lymphoma with combination chemotherapy suggests new relationships between these conditions as well as new possibilities for the treatment of acquired forms of intestinal lymphangiectasis associated with overwhelming gastrointestinal protein loss.

Adult↗
PubMed1980

The role of the prostaglandin system in the regulation of renal function in normal women.

The role of prostaglandins in the regulation of renal function was studied in seven healthy female volunteers taking a constant metabolic diet containing 59 meq of sodium and about 50 meq of potassium daily. Each subject underwent two renal clearance studies, during which vasopressin (priming dose, 200 mU; "sustainer," 200 mU/hour at 1 ml/min) was infused intravenously. The first clearance study served as the control; indomethacin (2 mg/kg/day) was given for seven days before the second clearance study to inhibit prostaglandin synthesis. Food and fluid were withheld for 12 hours before the studies. Urine was collected through an indwelling bladder catheter at 30 minute intervals. Glomerular filtration rate was estimated from inulin clearance and renal blood flow from para-aminohippurate (PAH) clearance. Indomethacin was associated with a significant increase in maximal urinary osmolality from 826 +/- 47 mosmol/kg H2) to 920 +/- 32 mosmol/kg H2O (P < 0.01). Minimal "free water" clearance was -1.40 +/- 0.02 ml/min before and -1.63 +/- 0.04 ml/min (P < 0.01) after the administration of indomethacin. Indomethacin did not affect urine flow, urinary sodium or potassium excretion, glomerular filtration rate or renal plasma flow. In addition, indomethacin did not affect the urinary excretion of cyclic adenosine monophosphate (AMP). Plasma arginine-vasopressin, measured in two subjects by radioimmunoassay, did not change with blockade of prostaglandin synthesis. It appears that prostaglandins antagonize the hydro-osmotic effect of antidiuretic hormone by an intrarenal mechanism, independent of changes in renal hemodynamics or cation excretion. This mechanism is probably mediated by an alteration in the water permeability of the collecting ducts. Since urinary cyclic AMP did not change during blockade of prostaglandin synthesis, whereas urinary osmolality increased, a change of vasopressin-dependent cyclic AMP production in the kidney was probably not reflected in urinary cyclic AMP.

Adult↗
PubMed1980

Effects of moderate short-term potassium depletion in normal humans. The role of prostaglandins.

The role of prostaglandins (PG) in the effects of potassium (K+)depletion was studied in six normal women. A mean K+-deficit of 220 mEq was induced with and without concomitant treatment with indomethacin (150 mg/day). Mean serum K+ concentration decreased from 4.2 +/- (S.E.) 0.1 to 3.2 +/- 0.1 mEq/L without indomethacin and from 4.1 +/- 0.1 to 3.2 +/- 0.1 mEq/L with indomethacin. "Supine" and "upright" plasma renin activity (PRA) and plasma norepinephrine concentration (NE) were unaltered by K+ -depletion alone but decreased with indomethacin. Plasma aldosterone (PA) was suppressed during K+-depletion (control: 7.2 +/- 2.6 ng/dl supine, 19.3 +/- 8.1 ng/dl upright; K+-depletion: 2.6 +/- 0.3 ng/dl supine, 5.5 +/- 1.3 ng/dl upright) and was paralleled by a decrease in urinary aldosterone. K+- depletion decreased urinary PGE2 from 667 +/- 133 to 343 +/- 60 ng/day (P less than 0.025) without a change in PGF2 alpha. The dose of exogenous angiotensin II (A II) which increased diastolic blood pressure by 20 mm Hg (pressor dose) was 7.1 +/- 1.4 ng/kg/min during control and increased to 11.0 +/- 0.7 ng/kg/min during K+-depletion (P less than 0.05). Indomethacin increased the sensitivity to A II both during control (pressor dose: 4.9 +/- 0.6 ng/kg/min) and K+ - depletion (pressor dose: 6.0 +/- 1.0 ng/kg/min). These results indicate that in healthy subjects, moderate short-term K+-depletion does not affect PRA or NE but decreases production of aldosterone and PGE2 by the kidney. The changes in vascular sensitivity to exogenous A II during K+-depletion and indomethacin and the decreases in plasma NE and PRA during indomethacin may be explained by changes in vascular vasodilator PG.

Aldosterone↗
PubMed1980

Correction of increased prostacyclin synthesis in Bartter's syndrome by indomethacin treatment.

The role of prostacyclin and thromboxane A2 in the pathogenesis of Bartter's syndrome was investigated by measurement of the urinary excretion of 6-keto-PGF1 alpha and thromboxane B2, respectively, in five patients. The prostaglandin metabolites were extracted from urine by a reproducible method and measured by specific radioimmunoassays. The patients with Bartter's syndrome excreted about four-times as much 6-keto-PGF1 alpha as the normal controls. In contrast, there was no significant difference in the urinary excretion of thromboxane B2 between the patients and the controls. In a second part of the study, three patients were treated with indomethacin (150 mg/day for four days), an inhibitor of prostaglandin synthesis. This regimen suppressed urinary excretion of 6-keto-PGF1 alpha by 43% and that of thromboxane B2 by 46%. It is suggested that the increase in prostacyclin production is responsible for both the hyperreninemia and and the other endocrine derangements as well as the hyporesponsiveness of blood pressure to intravenous infusion of vasopressors in patients with Bartter's syndrome.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

The role of urinary prostaglandin E and cyclic AMP in the polyuria of hypokalemia in rats.

The effect of potassium depletion on urinary prostaglandin E and cyclic AMP excretion was studied in female Sprague-Dawley and in Brattleboro rats. The animals were fed a potassium-free diet for 20 days which resulted in an average decrease in serum potassium of 25% in both strains. In the Sprague-Dawley rats, potassium depletion increased urine volume from 5.5 +/- 0.9 ml/day to 25.9 +/- 3.5 ml/day (p less than 0.001), decreased urinary osmolality from 1483 +/- 87 mosmol/kg H2O to 372 +/- 12 mosmol/kg H2O (p less than 0.001) and suppressed urinary cyclic AMP excretion from 56.95 +/- 3.81 nmoles/day to 0.83 +/- 0.40 nmoles/day (p less than 0.001). Potassium depletion in the Brattleboro rats did not affect these parameters. Excretion of prostaglandin E-like immunoreactivity in urine did not change in either strain with potassium depletion. The findings support the hypothesis that prostaglandins do not play a significant role in the polyuria caused by potassium deficiency in rats. Hypokalemia may cause polyuria by suppression of vasopressin-sensitive cyclic AMP generation, leading to a decrease in water permeability.

Animals↗
PubMed1980

Prostacyclin has effects on proximal and distal tubular function in the dog.

The effect of prostacyclin (PGI2), the major metabolite of arachidonic acid in arterial and venous tissue, on renal function was studied in hypophysectomized dogs under conditions of a maximum water diuresis. PGI2 (0.04 microgram/kg/min) significantly increased urine flow and urinary sodium and potassium excretion without affecting glomerular filtration rate. In addition, PGI2 significantly increased free water clearance and distal delivery of sodium and inhibited distal fractional reabsorption of glomerular filtrate. This suggests an effect of PGI2 on proximal as well as distal segments of the nephron. PGI2 is about 10 times more potent than PGE2 with regard to natriuresis and diuresis when studied under identical conditions. Thus, PGI2 may be the major prostaglandin involved in salt and water excretion.

Animals↗
PubMed1980

Indomethacin increases leucocyte beta-adrenoreceptors in man.

1. The effect of indomethacin, an inhibitor of prostaglandin synthesis, on number and sensitivity of alpha- and beta-adrenoreceptors was studied in normal healthy volunteer subjects. 2. The subjects were studied under metabolic conditions. To achieve inhibition of prostaglandin synthesis indomethacin (2 mg day-1 kg-1) was given orally for 7 days. This dose decreased urinary excretion of prostaglandin E-like immunoreactivity by 70%. 3. The number or alpha-adrenoreceptors was measured by the specific binding of [3H]dihydroergocryptine to platelet membranes and that of beta-adrenoreceptors by the binding of [3H]dihydroalprenolol to leucocyte membranes. 4. The number of alpha-adrenoreceptors did not change with indomethacin, nor did basal, prostaglandin E1- or noradrenaline-stimulated cyclic AMP production by platelet membranes. In contrast, the number of beta-adrenoreceptors increased by 92%. Indomethacin did not affect, however, basal, 1-isoprenaline- or prostaglandin E1-stimulated cyclic AMP production in leucocyte membranes. 5. These results suggest that a reflex-mediated decrease in sympathetic discharge in response to an indomethacin-induced decrease in release of vasodilator prostaglandins may lead to an 'up-regulation' of beta-adrenoreceptor sites.

Adult↗
PubMed1980

Dissociation between central and peripheral noradrenergic activity in essential hypertension.

1. Eleven patients with essential hypertension and nine healthy normotensive volunteer subjects, all without a neurological disorder, had blood drawn and cerebrospinal fluid sampled for analysis of noradrenaline (NA). 2. Cerebrospinal fluid NA levels were elevated (P < 0.01) in the hypertensive patients but plasma levels of NA were similar between groups. 3. The results suggest there is noradrenergic hyperactivity in the central nervous system which is not reflected in abnormal peripheral sympathetic nervous system function in this group of patients.

Adult↗
PubMed1980

Effect of prostacyclin (PGI2) on renal function and renin secretion in hypophysectomized dogs.

The effect of PGI2, the principal metabolite of arachidonic acid in mammalian arterial and venous tissues, on renal function and renin secretion was investigated in anesthetized, hypophysectomized dogs undergoing a maximal water diuresis. PGI2 in a concentration of 0.04 microgram/kg/min significantly increased urine flow and urinary sodium and potassium excretion in the absence of changes in glomerular filtration rate or blood pressure. The fact that PCI2 significantly increased free water clearance and distal delivery of sodium and inhibited distal fractional rea0sorption of glomerular filtrate is suggestive of an effect on proximal as well as distal sites of the nephron. PGI2 increased renin secretion rates threefold. This promotion of renin release may have been caused by an increase of ion flux across the macula densa or by an increase in renal blood flow. On a molar basis, PGI2 is about 10 times more potent than PGE2 with regard to natriuresis, diuresis and renin release when studied under identical conditions. Thus, PCI2 may be the major prostaglandin involved in the regulation of salt and water excretion.

Animals↗
PubMed1980

Nephropathologic characteristics of a woman with Bartter's syndrome after prolonged treatment with spironolactone.

A study was made of two renal biopsy specimens obtained from a 22-year-old woman with Bartter's syndrome, the first to substantiate the diagnosis, the second 2 years later after the treatment with spironolactone. The first renal biopsy revealed remarkable hyperplasia and hypertrophy of the juxtaglomerular apparatus. The numerous proliferating cells were characterized by abundant lysosomal granules and dilated endoplasmic reticulum. The macula densa revealed slight proliferation, with narrow intercellular space. The ultrastructural picture of the second biopsy specimen showed increased lipofuscin-like granules in the juxtaglomerular cells, with epitheloid cells of the macula densa showing degeneration and irregular dilatation of the intercellular spaces. However, the light microscopic finding was compatible with that of the first. These findings suggest that the treatment was inadequate although clinical features or biochemical laboratory data were improved.

Adult↗