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PubMed1990

Peripheral action of spironolactone: improvement in arterial elasticity.

Arterial elasticity, which can be assessed by means of a piezogram, is thought to be involved in the development of hypertension. In hypertensive patients (and with aging in normal subjects), arterial elasticity is reduced. Long-term administration of spironolactone, beta blockers, or a beta-blocker/dihydralazine combination to hypertensive patients sufficiently reduced systolic and diastolic blood pressure to about the same extent; however, only spironolactone had any effect on piezoelectric indexes of arterial elasticity.

Adrenergic beta-Antagonists↗
PubMed1990

Spironolactone and altizide used in combination with enalapril: twenty-four-hour ambulatory recording of blood pressure.

The addition of enalapril or acebutolol to a regimen of altizide + spironolactone in patients with moderate hypotension was investigated in a multicenter study of 53 patients. The patients underwent semiambulatory 24-hour blood pressure monitoring, especially to observe hypotensive episodes. In the 25 patients uncontrolled with altizide + spironolactone alone, enalapril and acebutolol were about equally effective in reducing blood pressure. The incidence of hypotension was low and comparable for both treatment groups, provided that the initial dose of angiotensin-converting enzyme inhibitor was low (5 mg).

Acebutolol↗
PubMed1990

Spironolactone versus nifedipine in essential hypertension.

In a double-blind, randomized, multicenter study of 194 patients with moderate hypertension, spironolactone and nifedipine were found to reduce blood pressure (BP) to about the same extent and in the same percentage of patients after 45 days of treatment (47 and 50%, respectively). At that point, the patients controlled by either drug continued on their regimen for another 45 days, while patients whose BP was still elevated (diastolic BP greater than 90 mm Hg), received the other drug in addition. After 45 days of combination therapy, 63% of the patients had normal BP, whereas those receiving monotherapy largely remained normotensive (96% in the spironolactone group and 88% in the nifedipine group). The adverse effects were not severe with either group, but the incidence was markedly higher in the nifedipine group.

Blood Pressure↗
PubMed1987

The influence of enalapril or spironolactone on experimental cyclosporin nephrotoxicity.

Adult Sprague-Dawley rats treated daily for 14 days with 50 mg/kg cyclosporin A (CsA) exhibited nephrotoxicity, characterized by reduced glomerular filtration rate, decreased urinary sodium and potassium flow, tubular enzymuria and proximal tubular structural damage. Elevations in plasma renin activity (PRA) were observed on day 4, but returned to normal within 7 days. Co-treatment of animals for the 14 day period with enalapril (8 mg/kg/day), a potent inhibitor of angiotensin converting enzyme (ACE), or spironolactone (25 mg/kg/day), the distal tubular antagonist of aldosterone, reduced the nephrotoxicity, although PRA remained elevated. Neither enalapril nor spironolactone affected circulating CsA levels. These data suggest that the action of aldosterone on the distal tubule may be important in the pathogenesis of CsA nephrotoxicity.

Acetylglucosaminidase↗
PubMed1984

Effect of spironolactone on electrolytes, renin, ACTH and corticosteroids in the rat.

Spironolactone (S), known to act as a mineralocorticoid antagonist, has been shown in some circumstances to inhibit steroid biosynthesis. To investigate these two actions in vivo in the rat, animals fed a normal or low Na+ diet were treated with S for 7 days. In animals fed a normal Na+ diet, urinary and faecal electrolytes, aldosterone and corticosterone excretion were measured daily, plasma renin, aldosterone, corticosterone, ACTH, progesterone, DOC and 18-OH-DOC were determined after 4 and 7 days of treatment. In animals fed a low Na+ diet, urinary electrolytes were measured daily and plasma and urinary aldosterone and corticosterone were determined at intervals during the introduction of the diet and in the course of treatment. On a normal Na+ diet, S induced a slight non significant rise in the urinary Na+/K+ ratio on the first day of treatment, no change in faecal electrolyte excretion, and a sustained increase in aldosterone but not in corticosterone excretion. It produced a 6-fold elevation in plasma aldosterone levels, a less marked rise in renin and progesterone, a delayed increase in DOC and no change in ACTH, 18-OH-DOC or corticosterone concentration. On a low Na+ diet, treatment induced a rise in the urinary Na+/K+ ratio, and in urine and plasma aldosterone levels and no change in corticosterone values. Our results confirm, in the intact rat, the antimineralocorticoid action of S characterized by an increase in Na+ excretion but no change in K+ elimination. No inhibitory effect of spironolactone on aldosterone, corticosterone or 18-OH-DOC biosynthesis could be demonstrated in our experimental model.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Effects of adrenalectomy and spironolactone on urinary metabolites of aldosterone in rats.

The quantities and temporal sequences of appearance of aldosterone metabolites in the urine of adrenalectomized rats, and adrenalectomized rats treated with spironolactone, were compared following subcutaneous administration of a physiological dosage (0.05 microgram) of [1,2,-3H]aldosterone. Large amounts of radiometabolites were rapidly excreted during 0-1 and 1-3 h and only small quantities by 3-4 h in urine of both groups of rats. The majority of the urinary radiometabolites (70-85%) were identified by Sephadex DEAP-LH-20 chromatography as neutral metabolites of aldosterone (NMA), together with lesser quantities of acidic, sulfate, and glucuronide conjugates. Further characterization by high pressure liquid chromatography (HPLC) showed that 90% of the NMA excreted by adrenalectomized rats were polar metabolites which could be separated into at least 15 peaks eluting in regions of increasing polarity (designated A, B, C, and D). Only small quantities of unaltered [3H]aldosterone and no ring-A-reduced metabolites were excreted by the adrenalectomized rats. Spironolactone treatment caused large changes in the excretion of acidic and sulfate derivatives of aldosterone, as well as discrete alterations in the HPLC patterns of the polar NMA (particularly those metabolites in regions A and B). Such discrete changes in these metabolic pathways which occur at the same time as the hormonal actions of aldosterone in the kidney may provide further insight into understanding the biological role of aldosterone metabolism.

Adrenal Glands↗
PubMed1984

The influence of age and multimorbidity on the pharmacokinetics and metabolism of spironolactone.

The pharmacokinetics of the metabolites of spironolactone (canrenone and fluorigenic metabolites) were investigated in 10 geriatric female patients with multimorbidity after a multiple daily oral administration of 100 mg spironolactone under steady state conditions. The concentration determinations were carried out simultaneously with a specific HPLC method and a less specific fluorimetric method. On comparison of the pharmacokinetic parameters with the respective values of a control group of younger healthy female subjects, the serum concentrations in the elderly patients were found to be twice as high. In addition, a statistically significant positive correlation with age was found in the patients for the kinetic parameters investigated. A positive correlation existed between erythrocyte count and the pharmacokinetic parameters of canrenone, especially with the area under the concentration/time curve. No such association was detectable, however, for the total fraction of fluorigenic metabolites (including canrenone). The results of our investigation indicate that, in addition to the known high binding of canrenone to plasma proteins, there is also possibly a (restrictive) binding to erythrocytes.

Aged↗
PubMed1991

Spironolactone in dermatologic therapy.

In the treatment of androgen-mediated skin disorders spironolactone provides a valuable therapeutic option. This article reviews the use of spironolactone as an antiandrogen in dermatologic therapy. The endocrinologic effects, pharmacology, dermatologic uses, and side effects are discussed, and guidelines for its use are provided.

Acne Vulgaris↗
PubMed1994

High-performance liquid chromatographic determination of spironolactone and its major metabolite canrenone in urine using ultraviolet detection and column-switching.

A rapid and simple column liquid chromatographic method involving a column-switching system for the determination of spironolactone and its main metabolite canrenone in urine is described. Purification and concentration was performed using an Hypersil ODS-C18, 30 microns (20 x 2.1 mm I.D.) pre-column. The most polar urinary compounds were removed by washing the pre-column with water, and the analytes were subsequently switched to a LiChrospher RP C18, 5 microns (125 x 4 mm I.D.) analytical column and separated by means of an acetonitrile-water mobile-phase. Under the proposed conditions, the extraction efficiency was approximately 100% over the 0.5-10.0 micrograms/ml concentration range. The limits of detection were 20 ng/ml for both compounds. The proposed method has been applied to urine samples obtained after the oral administration of spironolactone.

Canrenone↗
PubMed2006

Effect of spironolactone on C-reactive protein levels in patients with heart disease.

Animal evidence shows that aldosterone is pro-inflammatory and that aldosterone blockade is anti-inflammatory. Therefore part of the beneficial effect of aldosterone blockade that might contribute to it reducing mortality could be an anti-inflammatory effect. However, there are no previous data on whether aldosterone blockade is anti-inflammatory in man. We performed 4 separate studies to investigate whether spironolactone treatment would reduce levels of C-reactive protein (CRP), a marker of inflammation, in serum samples taken from patients suffering from different degrees of heart failure. We found in all 4 studies that spironolactone had no significant effect compared with placebo, on CRP levels in these patients. These studies provide evidence against the hypothesis that the clinical benefits produced by aldosterone blockade are due to it having anti-inflammatory effects.

Biomarkers↗
PubMed1981

Clinical evaluation of the effects of combined treatment with bromocriptine and spironolactone in two women with the polycystic ovary syndrome.

Two women with the polycystic ovary syndrome were treated with bromocriptine (15 to 20 mg/day) in combination with spironolactone (100 mg/day). In the first woman the combined therapy induced a marked reduction of hirsutism, with ensuing ovulation and pregnancy. In the second woman, who had hyperthecosis and had been refractory to treatment with clomiphene and wedge resection, the combined therapy resulted in abolition of hirsutism, normalization of blood pressure, weight reduction, and improvement in glucose intolerance. In this patient fertility could not be established by the above treatment, but the symptomatic amelioration was so great that she accepted no further attempt to induce ovulation. In view of the marked amelioration of the polycystic ovary syndrome induced by combined bromocriptine and spironolactone treatment, this mode of therapy should receive further consideration.

Adult↗
PubMed1981

Induction of ovulation with spironolactone (Aldactone) in anovulatory oligomenorrheic and hyperandrogenic women.

Thirteen anovulatory oligomenorrheic, hyperandrogenic, and normoprolactinemic women were treated with spironolactone (aldactone) throughout six consecutive menstrual cycles in a dosage of 100 to 150 mg/day. During this treatment a significant decrease in serum luteinizing hormone (LH), testosterone, prolactin, and 17-ketosteroid values were observed that were accompanied by ovulation in 11 women (85%), according to basal body temperature (BBT) and progesterone values. In addition, improvement of hirsutism was observed in 9 (70%) and restoration of regular cycles in 11 (85%) of the patients. The side effects observed were mild and did not lead to interruption of the treatment. Our data suggest that the antiandrogenic properties of spironolactone render it a suitable agent in the treatment of anovulatory, oligomenorrheic, and hyperandrogenic women.

17-Ketosteroids↗
PubMed1986

Spironolactone-reversible rickets associated with 11 beta-hydroxysteroid dehydrogenase deficiency syndrome.

A 7-year-old girl had growth retardation, hypertension, and hypokalemic alkalosis. Baseline serum aldosterone concentration and plasma renin activity were low and unresponsive to sodium deprivation and to orthostatic changes. Baseline serum progesterone, 17-hydroxyprogesterone, 11-deoxycortisol, and cortisol levels were normal and adequately responsive to ACTH stimulation. No steroid was found abnormally elevated. A diagnosis of 11 beta-hydroxysteroid dehydrogenase deficiency was established on the basis of elevated urinary tetrahydrocortisol plus allotetrahydrocortisol/tetrahydrocortisone ratio, determined by gas chromatography-mass spectrometry. Evaluation of bone mineral metabolism and parathyroid function, and skeletal radiographs, revealed the presence of rickets and secondary hyperparathyroidism. Treatment with spironolactone alone for 2 months corrected hypertension, hypokalemic alkalosis, and all laboratory and radiologic evidence of rickets and hyperparathyroidism, resulting in acceleration of growth rate. The response to spironolactone suggests that a hypermineralocorticoid state is responsible for the hypertensive syndrome and that rickets and hyperparathyroidism could be a consequence of excess mineralocorticoid activity.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1983

The effect of spironolactone on the elemental composition of the intraluminal fluids of the seminiferous tubules, rete testis and epididymis of the rat.

Embryologically, the epididymis and renal collecting tubules develop from the mesonephric duct. Aldosterone enhances the reabsorption of sodium from the collecting tubule, and there is evidence that sodium is removed from the epididymal lumen against a concentration gradient. Rats were treated with spironolactone, an aldosterone antagonist, and the concentrations of seven elements, including sodium, were measured in intraluminal fluids from the testis and epididymis. The sodium concentration in caput epididymidal fluid rose (102.5 +/- 4.4 to 128.0 +/- 6.8 mmol./l., p less than 0.01) after 14 days of spironolactone treatment. This finding is consistent with the hypothesis that aldosterone acts on the caput epididymidis, like the collecting tubule, to augment the removal of sodium from luminal fluid.

Animals↗
PubMed1978

Antiandrogenic effects of spironolactone: hormonal and ultrastructural studies in dogs and men.

A decrease in the level of plasma testosterone and an increase in the level of plasma progesterone were noted after spironolactone had been administered for 20 days in 5 patients with prostatic carcinoma, as well as in 8 male dogs. Electron microscopic observation disclosed myelin-like bodies in the cytoplasm of Leydig and adrenocortical cells in dogs, contributing to a resolution of the mode of antiandrogenic action of spironolactone.

Adrenal Glands↗
PubMed1975

Suppression of plasma androgens by spironolactone in castrated men with carcinoma of the prostate.

Spironolactone, an inhibitor of androgen synthesis, has been administered to castrated men with metastatic carcinoma of the prostate. Plasma levels of testosterone, androstenedione and dehydroepiandrosterone were significantly decreased. These data indicate that spironolactone suppresses adrenal androgen production and suggest that it may be of benefit in the treatment of orchiectomized patients with advanced carcinoma of the prostate.

Aged↗