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At least 19 recordsLinked to original sources
PubMed1975

Assessment of urine-concentrating ability in man: effect of fludrocortisone and urea in enhancing response to vasopressin.

1. Healthy subjects, given a long-acting preparation of vasopressin intramuscularly, excreted a significantly less concentrated urine than when subjected to fluid deprivation for 28 h. 2. When fludrocortisone, a potent mineralocorticoid, was given in addition to vasopressin the urine was not significantly less concentrated than after fluid deprivation. 3. Oral urea-loading also enhanced the urine-concentrating power of vasopressin but its effect was less marked than that of fludrocortisone. Oral urea did not increase further the urine concentration achieved by combined fludrocortisone and vasopressin. 4. Renal concentrating power was assessed in fourteen patients with renal disease and impaired concentrating ability. Fludrocortisone significantly enhanced the urine concentration achieved by vasopressin alone and the resultant urine was not significantly less concentrated than that achieved by fluid deprivation. 5. The action of fludrocortisone in enhancing the urine-concentrating effect of vasopressin is similar to that of aldosterone and is probably due to the increased sequestration of solute in the renal medulla, caused by increased reabsorption of sodium chloride in the ascending limb of the loop of Henle. 6. In the clinical assessment of renal concentrating power, the combined use of fludrocortisone and vasopressin has potential advantages over established methods.

Adolescent↗
PubMed1979

The pressor actions of noradrenaline, angiotensin II and saralasin in chronic autonomic failure treated with fludrocortisone.

1 Treatment of postural hypotension due to chronic autonomic failure with fludrocortisone increased the pressor sensitivity to intravenous noradrenaline. Fludrocortisone increased the blood pressure in the standing but not the lying position. These effects of fludrocortisone may be the result of increased sensitivity of vascular receptors to noradrenaline. 2 The pressor action of angiotensin II, to which patients were supersensitive, may have involved the stimulation of alpha-adrenoceptors since it was partially antagonised by phentolamine. 3 Saralasin had a marked, paradoxical, pressor effect. This may have been mediated by vascular alpha-adrenoceptors because log dose-response curves of saralasin-induced increases in systolic pressure were shifted to the right in a parallel fashion after phentolamine. 4 Fludrocortisone treatment increased the pressor sensitivity to intravenous saralasin but not to angiotensin-II.

Aged↗
PubMed1976

Therapeutic experience with fludrocortisone in diabetic postural hypotension.

Fourteen patients with diabetic postural hypotension were treated with fludrocortisone for a mean 12 months (range 6-30 months). The mean daily dose of fludrocortisone was 0.2 mg (range 0.1 mg-0.4 mg). Standing systolic and diastolic blood pressures increased significantly (P less than 0.001) after treatment with fludrocortisone and the postural hypotension decreased significantly (P less than 0.001). Thirteen patients noted considerable symptomatic improvement. Fludrocortisone should be used cautiously in patients with congestive cardiac failure or the nephrotic syndrome.

Adult↗
PubMed1975

Levodopa-induced postural hypotension. Treatment with fludrocortisone.

Six parkinsonian patients with symptomatic postural hypotension secondary to levodopa therapy were treated with 0.05 to 0.2 mg of fludrocortisone acetate daily for six to ten months. Severe orthostatic light-headedness and frequent syncope had previously been alleviated only be reducing the dosage of levodopa to levels producing less than optimal antiparkinsonian benefits. In all six patients, symptoms were alleviated satisfactorily, and supine and upright blood pressures returned to normal levels during treatment with fludrocortisone acetate. There were no adverse reactions. Fludrocortisone acetate is an effective and safe drug for the treatment of severe and otherwise intractable postural hypotension secondary to therapy with levodopa.

Aged↗
PubMed1975

Response of plasma aldosterone to fludrocortisone in primary hyperaldosteronism and other forms of hypertension.

The response of plasma aldosterone to fludrocortisone administration (400 mug 12-hourly for 3 days) was studied in twenty-two patients with primary hyperaldosteronism. No difference was observed in the response between those patients with an adrenal adenoma and those with bilateral adrenocortical hyperplasia, there being no significant change in plasma aldosterone levels across the test period. No separation between the groups was seen when basal plasma renin concentration was related to the aldosterone level following fludrocortisone. It is concluded that the test is of little value in the pre-operative differentiation of these conditions. Twenty-three patients with no demonstrable cause for their hypertension and four with elevated levels of plasma deoxycorticosterone were similarly studied for comparison. These groups demonstrated a normal fall in plasma aldosterone levels following fludrocortisone.

Adenocarcinoma↗
PubMed1978

Semiautomated system for high-pressure liquid chromatographic determination of dissolution rate of fludrocortisone acetate tablets.

A new semiautomated high-pressure liquid chromatographic (HPLC) system is described to determine the dissolution rate of fludrocortisone acetate tablets. The system uses a miniaturized dissolution basket and shaft assembly having the same geometry as that given in USP XIX. This reduced size permits use of smaller volumes of dissolution medium, allowing most very low dose oral solid dosage forms to be handled. The USP dissolution kettle was also replaced with a new miniaturized vessel that continuously filters the sample solution before it enters the flow system. Volumes of dissolution medium as small as 15 ml can be accommodated, depending on the sensitivity of the assay employed and the solubility of the drug substance under study. The concentration of fludrocortisone acetate in solution was monitored by a new HPLC system employing a reversed-phase column compatible with the aqueous dissolution medium used. A comparative dissolution study of different lots was made using different basket rotation speeds.

Autoanalysis↗
PubMed1975

[Fludrocortisone in the treatment of orthostatic hypotension: ophthalmodynamography during standing(author's transl)].

The effect of fludrocortisone (Astonin -H) in the management of orthostatic hypotension was tested in a double-blind trial of 30 patients who were receiving 0.3 mg fludrocortisone for seven days, a control group of 30 subjects receiving placebos. Systolic and diastolic brachial and ophthalmic arterial pressures, pulse amplitude and pulse rate were measured at rest, immediately after standing up and 10 minutes later. Comparing the treatment and placebo groups, the former had a higher systolic ophthalmic blood pressure on standing, a smaller fall of pulse volume and less of a rise in heart rate on standing up, and a raised systolic brachial artery pressure even in recumbency. At the same time there was an improvement in symptoms.

Adult↗
PubMed1979

Analysis of fludrocortisone acetate and its solid dosage forms by high-performance liquid chromatography.

A newly developed reversed-phase high-performance liquid chromatographic assay and test method for determining content uniformity are described for fludrocortisone acetate. The method is stability indicating and separates most known degradation products and impurities. In addition, the method is simple, sensitive, accurate, and relatively free of interferences. The coefficient of variation for multiple weight assays is between 0.3 and 1.8%.

Chromatography, High Pressure Liquid↗
PubMed1977

Amelioration of metabolic acidosis with fludrocortisone therapy in hyporeninemic hypoaldosteronism.

In four patients with renal hyperchloremic acidosis and hyperkalemia, hyporeninemic hypoaldosteronism and chronic renal insufficiency (glomerular filtration rates of 13, 31, 35 and 44 ml per minute per 1.73 m2), prolonged administration of fludrocortisone increased urinary potassium and net acid excretion, corrected hyperkalemia and substantially ameliorated acidosis. Except in the patient with the lowest glomerular filtration rate, the increased net acid excretion was due mostly to increased ammonium excretion. Urine pH decreased initially in each patient, but in the three patients with the highest filtration rates, it increased subsequently as ammonium excretion increased, indicating that renal ammonia production increased. Urinary ammonium excretion correlated inversely with serum potassium concentration and did not decrease on discontinuation of therapy if hyperkalemia was prevented from recurring. In patients with renal acidosis and hyporeninemic hypoaldosteronism, administration of mineralocorticoid hormone can augment both renal hydrogen-ion secretion and, by correction of hyperkalemia, renal ammonia production, and thereby ameliorate metabolic acidosis.

Acidosis, Renal Tubular↗
PubMed1976

The pharmacodynamics of single doses of prorenoate potasssium and spironolactone in fludrocortisone treated normal subjects.

1 The pharmacodynamic profile of single oral doses of prorenoate potassium (40 mg) and spironolactone (100 mg), as judged by reversal of the effects of fludrocostisone on the urinary electrolyte composition, was compared to that of placebo in a double-blind crossover study in six healthy subjects. 2 Both drugs showed evidence of significant activity in all periods between 2-16 h after treatment, and the time course of their activity was very similar. 3 In the total 24 h period after treatment both drugs significantly increased sodium excretion, the Na/K ratio and the log 10 Na/K ratio over placebo values, and urine potassium concentration was significantly reduced. Changes in urine volume and in potassium excretion were not significant. 4 The responses to prorenoate potassium (40 mg) were not significantly different from those to spironolactone 100 mg), and were very similar as judged by the urine log 10 Na/K ratio, indicating that the two drugs were approximately equiactive at these doses. 5 Reductions in urinary potassium excretion, when expressed in relation to the amount of sodium excreted, were significantly larger after prorenoate potassium than after spironolactone, confirming a qualitative difference in the pharmacological activity of the two drugs which has been reported previously.

Administration, Oral↗