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Biomedical subjects

F C Bartter

Publications and source records attributed to F C Bartter.

At least 91 records · Page 5Linked to original sources
PubMed1977

Primary hyperparathyroidism presenting as anticonvulsant-induced osteomalacia.

A patient presented with the classic features of anticonvulsant-induced osteomalacia. Following discontinuance of diphenylhydantoin therapy and repletion with physiologic quantities of vitamin D, hypercalcemia and persistent biochemical hyperparathyroidism developed, and a parathyroid adenoma was removed. A history of nephrolithiasis and hypercalcemia preceding the institution of drug therapy allowed this patient's underlying parathyroid disease to be defined as primary hyperparathyroidism, which had been obscured by anticonvulsant therapy.

Adenoma↗
PubMed1977

Renal changes in primary aldosteronism.

The clinical presentations and renal biopsy specimens of 18 patients with primary aldosteronism were reviewed to determine the characteristic pathologic features of the kidney in this syndrome. All patients were hypertensive with a mean blood pressure of 192 nm. Hg systolic and 122 mm. Hg diastolic. The average duration of hypertension was 6.88 years. The mean serum potassium was 2.88 mEq. per l. and the mean plasma carbon dioxide was 31.4 mEq. per l. A significant history of urinary tract disease was noted in 8 patients. Laboratory and diagnostic studies evaluating renal structure and function were abnormal in 11 patients. Renal biopsies from all 18 individuals showed evidence of parenchymal damage. Hypertensive and hypokalemic changes were the most significant abnormalities and were considered moderate to severe in 78 and 89 per cent of the patients, respectively. Histologic evidence of pyelonephritis was noted in 2 patients only and no renal specimens contained characteristic changes of metabolic alkalosis. The preoperatively hypertensive and renal evaluations did not reflect the severity of the renal changes noted histologically. The extent of renal injury caused by hypertension and hypokalemia in these patients emphasizes the consequences of primary aldosteronism. Early diagnosis and treatment of this disorder are essential if these consequences are to be avoided.

Adult↗
PubMed1977

Effect of propranolol on renin release in the dog.

Infusion of d,l-propranolol in both anesthetized and conscious dogs caused decreases in heart rate (HR), plasma renin activity (PRA), and plasma aldosterone. There was no consistent change in mean arterial blood pressure, plasma renin substrate concentration, packed cell volume, plasma potassium, or plasma sodium concentration following the infusion of propranolol. In five conscious animals, infusion of propranolol (1 mg/kg followed by 0.47-0.65 mg kg-1 h-1) reduced HR from 117.6 +/- 4.0 beats per minute (mean +/- SE) during control periods of 73.2 +/- 2.0 beats per minute (P less than 0.005) 90 min after the start of infusion. PRA decreased from 9.97 +/- 1.79 ng ml-1 h-1 during control periods to reach 1.50 +/- 0.42 ng ml-1 h-1 (P less than 0.005) at the end of the 90-min infusions. Plasma aldosterone also decreased during this time from 17.60 +/- 1.93 ng% during control periods to reach 6.64 +/- 0.98 ng% (P less than 0.005). The data suggest that propranolol at the dose administered suppresses renin and aldosterone secretion in unstimulated dogs. They suggest also that beta-receptor activity contributes to basal renin release.

Aldosterone↗
PubMed1977

Role of prostaglandins in the control of renin secretion in the dog.

Infusion of indomethacin into anesthetized, salt-depleted dogs cuased an increase in mean arterial blood pressure (MABP), and decreases in heart rate (HR), urine flow rate (V), renal plasma flow (RPF), and renin secretion rate. MABP was 112.1 +/-5.4 mm Hg during control periods and was 147.7 +/- 5.6 mm Hg (P less than 0.005) 80 minutes after the infusion of indomethacin. V was 0.38 +/- 0.06 ml/min during control periods and was 0.08 +/- 0.01 ml/min (P less than 0.005) 80 minutes after the infusion of indomethacin. RPF was 126.3 +/- 13.3 ml/min and 41.5 +/- 7.5 ml/min, respectively (P less than 0.005), before and after 80 minutes of infusion. Renin secretion rate decreased from 1,194.1 +/- 353.9 U/min during control periods to reach 384.0 +/- 125.8 U/min (P less than 0.025) by 80 minutes of infusion of indomethacin. Subsequent infusion of prostaglandin E2 (PGE2) into the renal artery for 80 minutes caused increases of V to 0.53 +/- 0.13 ml/min (P less than 0.01), of RPF to 102.4 +/- 23.1 ml/min (P less than 0.01), and of renin secretion rate to 2,582.6 +/- 786.4 U/min (P less than 0.005). The decrease in renin secretion rate during the infusion of indomethacin persisted when renal perfusion pressure (RPP) was maintained relatively constant before and during the infusion of indomethacin. Furthermore, we found that infusion of prostaglandin E1 (PGE1) into the kidney gave the same pattern of response as PGE2. The data suggest that PGE1 and PGE2 play a role in the control of renin secretion.

Animals↗
PubMed1977

Nephrogenous cyclic adenosine monophosphate as a parathyroid function test.

Nephrogenous cyclic AMP (NcAMP), total cyclic AMP excretion (UcAMP), and plasma immunoreactive parathyroid hormone (iPTH), determined with a multivalent antiserum, were prospectively measured in 55 control subjects, 57 patients with primary hyperparathyroidism (1 degrees HPT), and 10 patients with chronic hypoparathyroidism. In the group with 1 degrees HPT, NcAMP was elevated in 52 patients (91%), and similar elevations were noted in subgroups of 26 patients with mild (serum calcium </=10.7 mg/dl) or intermittent hypercalcemia, 19 patients with mild renal insufficiency (mean glomerular filtration rate, 64 ml/min), and 10 patients with moderate renal insufficiency (mean glomerular filtration rate, 43 ml/min). Plasma iPTH was increased in 41 patients (73%). The development of a parametric expression for UcAMP was found to be critically important in the clinical interpretation of results for total cAMP excretion. Because of renal impairment in a large number of patients, the absolute excretion rate of cAMP correlated poorly with the hyperparathyroid state. Expressed as a function of creatinine excretion, UcAMP was elevated in 81% of patients with 1 degrees HPT, but the nonparametric nature of the expression led to a number of interpretive difficulties. The expression of cAMP excretion as a function of glomerular filtration rate was developed on the basis of the unique features of cAMP clearance in man, and this expression, which provided elevated values in 51 (89%) of the patients with 1 degrees HPT, avoided entirely the inadequacies of alternative expressions. Results for NcAMP and UcAMP in nonazotemic and azotemic patients with hypoparathyroidism confirmed the validity of the measurements and the expressions employed.

Adolescent↗
PubMed1977

Renin-aldosterone profiling in hypertension.

Renin-aldosterone profiling was used to classify patients with hypertension: 243 patients with essential hypertension were classified by renin-urinary sodium indexing; 107 were reclassified by response to administration of furosemide and intravenous saline; 45 were further classified by response to a low-sodium diet. Arbitrary "normal ranges" were determined in 89, 32, and 38 volunteers, respectively. Patients with low-renin apparently do not have "high-volume" hypertension. Rather, they show a primary renal abnormality in renin secretion and become relatively deficient in angiotensin II and aldosterone when they are subjected to diuresis. They can maintain aldosterone secretion under normal conditions because their adrenal aldosterone receptor is supersensitive to angiotensin II. No evidence of abnormal sympathetic neural activity was found among the renin subgroups. Renin-aldosterone profiling in current clinical practice seems useful mainly in the detection of patients with curable forms of secondary hypertension. Aldosterone/renin ratios may be particularly helpful in diagnosis when obtained after a patient has undergone expansion or contraction of his extracellular fluid volume.

Aldosterone↗
PubMed1977

Bartter's syndrome.

The syndrome of juxtaglomerular hyperplasia with hypokalemic, hypochloremic alkalosis, aldosteronism, hyperreninemia, and normal blood pressure may be familial, and is probably inherited as a recessive trait. It can usually be distinguished from salt-losing chronic glomerulo-nephritis by the histologic appearance of the kidneys, and by the absence of sodium "leak" with a low-sodium intake. Urinary, and thus renal, prostaglandin E is increased in the untreated patient: when this is lowered with prostaglandin synthetase inhibitors, the plasma renin and aldosterone decrease, and the plasma potassium concentration rises. These and other results suggest a partial control of renin secretion by prostaglandin E, and also suggest that prostaglandin E is an essential feature of the syndrome; it may, indeed, be a "proximal" cause of all the essential features.

Adrenalectomy↗
PubMed1976

Bartter's syndrome: a disorder characterized by high urinary prostaglandins and a dependence of hyperreninemia on prostaglandin synthesis.

Urinary prostaglandins E2 and F2alpha were measured by gas chromatography-mass spectrometry in three adult women and an adolescent girl with Bartter's syndrome. On a constant metabolic diet prostaglandin E2 ranged from 293 to 1,221 ng/day (mean, 640 ng/day) and exceeded the normal range for adults of 76 to 281 ng/day in all patients. Prostaglandins F2alpha ranged from 291 to 1,061 ng/day (mean, 747 ng/day) in the adult women. Only in a young girl did prostaglandins F2alpha (1,677 ng/day) clearly exceed the normal range for adults of 422 to 871 ng/day. Treatment with indomethacin, which decreased urinary prostaglandin E-like material by 69 per cent or more, did not affect blood pressure. Plasma renin activity, which ranged from 5.2 to 22.2 ng/ml/hour (patients supine) and from 23.3 to 30.4 ng/ml/hour (patients upright), and urinary aldosterone, which ranged from 14.0 to 45.6 ng/day, decreased by 79, 65 and 52 per cent, respectively. The clearance of creatinine was lower for the eight or nine days of treatment, the balances of sodium and potassium were positive, and serum potassium was higher than in control. Ibuprofen, an inhibitor of prostaglandin synthetase which differs in structure from indomethacin, produced metabolic effects which were qualitatively similar to those of indomethacin. The results indicate that the renal synthesis of prostaglandins is increased in Bartter's syndrome and that prostaglandins mediate the hyperreninemia and hyperaldosteronism which characterize the disorder. The over-production of prostaglandins by the kidney could be proximal cause of the syndrome, or secondary to intrarenal changes of an unknown nature. This study provides additional evidence for an important role for prostaglandins in the release of renin.

Adolescent↗
PubMed1976

Control of calcium absorption: effect of sodium chloride loading and depletion.

In six out of eight patients with normal parathyroid function and in two subjects with hypoparathyroidism, sodium chloride loading was shown to increase calcium absorption as measured by the 47Ca absorption test. Although no significant change was seen in the renal and fecal excretion of calcium, a slight decrease in total serum calcium did occur with increased sodium intake. The change in calcium absorption was not accompanied by a detectable change in calcium balance. Therefore, a compensatory change in gastrointestinal calcium secretion must have occurred. Sodium intake has an effect on calcium in the gastrointestinal tract, which is independent of parathyroid hormone. Sodium intake should be considered when results of studies of calcium metabolism are compared.

Calcium↗
PubMed1976

Radioimmunoassays for aldosterone and deoxycorticosterone in plasma and urine.

Radioimmunoassays for aldosterone and deoxycorticosterone (DOC) are described in which a simple separation procedure using ammonium sulfate stabilization of bound steroid and extraction of free steroid into toluene scintillant allows an "in vial" assay without mechanical separation of the two phase system. Extraction and thin layer chromatographic methods for purification of aldosterone and DOC are free of solvent and plate blank effects. Normal values are given for unconjugated aldosterone and DOC in urine, for aldosterone and DOC in plasma and for aldosterone 18-glucuronide in urine.

Adrenal Gland Neoplasms↗
PubMed1976

Segmental renal vein renin assay and segmental nephrectomy for correction of renal hypertension.

Selective segmental renal vein catheterization was used to obtain venous blood samples for renin assay. With this technique a localized source of hypersecretion of renin was identified in 2 patients. Using samples from the main renal veins we found no significant difference in renin activity and, therefore, the etiology of the hypertension in these 2 patients would have been missed. Segmental nephrectomy resulted in a cure of the hypertension in both patients who were followed for a minimum of 14 months.

Adolescent↗