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Generic Aldactone is an effective medication which helps to fight with hyperaldosteronism, hypokalemia, edema, ascites, hirsutism, alopecia (baldness), acne. It can be also used together with other medicines to treat myasthenia gravis, precocious puberty, high blood pressure. Generic Aldactone acts by controlling the level of water and salt and by decreasing the potassium loss from your body.

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Also known as:  Spironolactone.


Generic Aldactone is a perfect remedy, which helps to fight with hyperaldosteronism, hypokalemia, edema, ascites, hirsutism, alopecia (baldness), acne. It can also be used together with other medicines to treat myasthenia gravis, precocious puberty, high blood pressure.

Generic Aldactone acts by controlling the level of water and salt and by decreasing the potassium loss from your body.

Aldactone is also known as Spironolactone, Spirotone, Spiractin, Osyrol, Spiroctan, Spirolon, Verospiron.

It is aldosterone receptor antagonists.

Generic name of Generic Aldactone is Spironolactone.

Brand names of Generic Aldactone are Aldactone, Spiractin, Spirotone, Spironol, Berlactone, Novo-Spiroton.


You can feel the effects of Generic Aldactone after 2 weeks of treatment. It depends on the health state and other factors of the patient.

Take Generic Aldactone tablets orally with water, at the same time every day.

Do not crush or chew it.

Take Generic Aldactone once (in the morning) or twice a day.

If you want to achieve most effective results do not stop taking Generic Aldactone suddenly.


If you overdose Generic Aldactone and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Aldactone overdosage: diarrhea, vomiting, nausea, red skin rash, loss of energy, slow heartbeat, weakness in legs, feeling drowsy, confusion.


Store below 25 degrees C (77 degrees F). Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Aldactone are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Aldactone if you are allergic to Generic Aldactone components.

Do not take Generic Aldactone if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Aldactone can harm your baby.

Do not take Generic Aldactone if you are taking potassium-sparing diuretics (such as Aldactazide, amiloride (Moduretic, Midamor)), triamterene (such as Maxzide, Dyazide, Dyrenium)).

Be careful using Generic Aldactone if you take inhibitors (enalapril (such as Vasotec), fosinopril (such as Monopril), captopril (such as Capoten), benazepril (such as Lotensin), lisinopril (such as Zestril, Prinivil), quinapril (such as Accupril), moexipril (such as Univasc), ramipril (such as Altace), trandolapril (such as Mavik)); oral steroids (dexamethasone (such as Decadron, Dexone), prednisone (such as Deltasone), methylprednisolone (such as Medrol)); aspirin and other nonsteroidal anti-inflammatory medicines (naproxen (such as Aleve, Naprosyn), ibuprofen (such as Advil, Motrin), indomethacin (such as Indocin)); diuretics; barbiturates, phenobarbital; digoxin (such as Digitek, Lanoxicaps, Lanoxin)); high blood pressure medicines, lithium (such as Lithobid, Eskalith); perindopril (such as Aceon).It can be dangerous to use Aldactone if you suffer from or have a history of liver disease, kidney disease, potassium high levels in your blood, problems with urination.

Be careful with this drug if you are going to have a surgery.

Avoid food with high level of salt.

Avoid dehydration.

Avoid medicines which cause lightheadedness.

You should be careful when you are driving or operating machinery.

Do not stop taking Generic Aldactone suddenly.

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Because of the prognostic importance of LV dysfunction following an AMI and the increasing use of electrical and/or mechanical interventions in patients with LV systolic dysfunction, this retrospective analysis of EPHESUS patients with LVEF

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The Study group on HF Awareness and Perception in Europe (SHAPE) surveyed randomly selected C (2041), I/G (1881), and PCP (2965) in France, Germany, Italy, the Netherlands, Poland, Romania, Spain, Sweden, and the UK. Each physician completed a 32-item questionnaire about the diagnosis and treatment of HF (left ventricular ejection fraction <40%). This report provides an analysis of HF awareness among C, I/G, and PCP. Seventy-one per cent I/G and 92% C use echocardiography, and 43% I/G and 82% C use echo-Doppler as a routine diagnostic test (both P < 0.0001). In contrast, 75% PCP use signs and symptoms to diagnose HF. Fewer I/G would use an angiotensin-converting enzyme (ACE)-inhibitor in >90% of their patients (64 vs. 82% C, P < 0.0001), whereas only 47% PCP would routinely prescribe an ACE-inhibitor. Worsening HF was considered a risk of ACE-inhibitor therapy by 35% PCP. I/G and PCP consistently do not prescribe target ACE-inhibitor doses (P < 0.0001 vs. C). Only 39% I/G would use a beta-blocker in >50% of their patients (vs. 73% C, P < 0.0001). Also, only 5% PCP would always, and 35% often, prescribe a beta-blocker and reach target doses in only 7-29%. Moreover, 34% PCP and 26% I/G vs. 11% C (P < 0.0001) do not start a beta-blocker in patients with mild HF, who are already on an ACE-inhibitor and are on diuretic. In mild, stable HF, 39% PCP and 18% I/G would only prescribe diuretics, vs. 7% C (P < 0.0001). In patients with worsening HF in sinus rhythm and on an optimal ACE-inhibitor, beta-blockade and diuretics, significantly more C would add spironolactone, but I/G would more often add digoxin.

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This is a two-center study conducted in university-based hypertension clinics directed by clinical hypertension specialists. Forty-six patients with resistant hypertension and stages 2 or 3 CKD (mean estimated glomerular filtration rate (eGFR) 56.5 + or - 16.2 ml/min/1.73 m(2)) were evaluated for safety and efficacy of aldosterone blockade added to preexisting BP-lowering regimens. All patients were on three mechanistically complementary antihypertensive agents including a diuretic and a renin-angiotensin system blocker. Patients were evaluated after a median of 45 treatment days. The primary endpoint was change in systolic BP. Secondary endpoints included change in serum potassium, creatinine, eGFR, diastolic BP and tolerability.

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Chromatography of steroidal spirolactones on DEAE-Sephadex A-25 under selected pH conditions allowed efficient separation of these compounds from other steroids and many of the endogenous components of human urine. The spirolactones were recovered in high yield, mostly over 90%. Lipophilic-gel chromatography provided a useful method for group fractionation of mixtures of these spirolactones with high recoveries (generally over 90%), unaffected by the presence of endogenous material from normal human urine.

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Eplerenone (a selective aldosterone blocker) or vehicle (control), was given to male Wistar rats (50 mg/kg, twice daily) for 7 days before unilateral ureteral obstruction (UUO) and for an additional 28 days after surgery. Body weight, blood pressure, renal histo-morphology, immune-staining for macrophages, monocyte chemotactic protein-1, proliferating cell nuclear antigen, α-smooth muscle actin, and serum and urine markers of renal function and oxidative stress were determined for both groups on 7, 14, and 28 days after surgery.

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Hyperstimulation appeared in one case on the 10th 11th day after ovulation, allowing by its presence the very precocious diagnosis of successful fecondation. The study of blood coagulation revealed that hypercoagulability was mainly related to hyperactivity of the thrombocytes and of the coagulation proteins. The pathogenesis of the syndrome is discussed. Increase in the permeability of the capillary vessels and hypovolemia seem to be responsible for the main accidents. Unfortunately as we have no real mean of decreasing the permeability of the capillary vessels, the treatment can be directed only against hypovolemia and its results. The infusion of macromolecular fluids, the restriction of sodium and water intake, together with the prescription of spironolactone have been successfully employed in those three cases.

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In this open study, the potassium-sparing diuretic spironolactone/altizide decreases LVM index in hypertensive patients, who were selected for follow-up because they had echocardiographic LVH and because their BP had normalised during an initial 2-month treatment period.

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In the ARB-treated group, aldosterone concentrations remained unchanged (1.10 +/- 0.20 nmol/l, compared with 1.17 +/- 0.46 nmol/l in the control group), whereas systolic blood pressure (178 +/- 9 mmHg), left ventricular weight (0.372 +/- 0.035 g/100 g body weight), expression of collagen mRNA, and cardiac interstitial and perivascular fibrosis all decreased significantly compared with the control group (systolic blood pressure: 222 +/- 10 mmHg, P < 0.05; left ventricular weight: 0.483 +/- 0.021 g/100 g body weight, P < 0.05). Although blood pressure (217 +/- 9 mmHg) and left ventricular weight (0.467 +/- 0.027 g/100 g body weight) remained unchanged in the group receiving spironolactone, the expression of both types of collagen mRNA and cardiac interstitial and perivascular fibrosis showed a significant decrease compared with the vehicle-treated group. In the rats receiving combined treatment with the ARB and spironolactone, left ventricular weight (0.352 +/- 0.005 g/100 g body weight, P < 0.05), expression of collagen mRNA, and cardiac interstitial and perivascular fibrosis all showed a further improvement compared with both the ARB and spironolactone groups.

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The time of follow-up was from 2 to 3 years and the average was 29 months. In the treatment group, the rate of recurrence of esophageal varices was 19.0% (8/42) and the average time was 30 months; the incidence of esophageal variceal bleeding was 11.9% (5/42) and 2 patients died. In the control group, the rate of recurrence of esophageal varices was 43.3% (13/30) and the average time was 18 months; the incidence of esophageal variceal bleeding was 36.7% (11/30) and 7 patients died. The therapeutic efficacy of the treatment group was much superior to that of the control group.

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The relative bioavailability was 99.2 ± 11.6% and 97.6 ± 7.4% under fasting and fed condition, respectively. The 90% confidence intervals of the adjusted geometric mean ratio (test/reference) of Cmax, AUC0-tlast, and AUC0-∞ were 89.7-113.8%, 93.9-103.3%, and 90.0-103.0% in fasting study and 87.7-102.3%, 95.1-99.5%, and 94.1-98.9% in fed study, respectively.

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Personal, social, and medical factors unique to individual patients have a bearing on the efficacy of specific antihypertensive agents and on the frequency and severity of side effects. The factors relate to age, sex, occupation, potential for adherence to a prescribed program of therapy, and associated health problems. The importance of a simple, inexpensive program is emphasized.

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Prior studies have linked renoprotective effects of estrogens to G-protein-coupled estrogen receptor-1 (GPER-1) and suggest that aldosterone may also activate GPER-1. Here, the role of GPER-1 in murine renal tissue was further evaluated by examining its anatomical distribution, subcellular distribution and steroid binding specificity. Dual immunofluorescent staining using position-specific markers showed that GPER-1 immunoreactivity primarily resides in distal convoluted tubules and the Loop of Henle (stained with Tamm-Horsfall Protein-1). Lower GPER-1 expression was observed in proximal convoluted tubules marked with megalin, and GPER-1 was not detected in collecting ducts. Plasma membrane fractions prepared from whole kidney tissue or HEK293 cells expressing recombinant human GPER-1 (HEK-GPER-1) displayed high-affinity, specific [(3)H]-17β-estradiol ([(3)H]-E2) binding, but no specific [(3)H]-aldosterone binding. In contrast, cytosolic preparations exhibited specific binding to [(3)H]-aldosterone but not to [(3)H]-E2, consistent with the subcellular distribution of GPER-1 and mineralocorticoid receptor (MR) in these preparations. Aldosterone and MR antagonists, spironolactone and eplerenone, failed to compete for specific [(3)H]-E2 binding to membranes of HEK-GPER-1 cells. Furthermore, aldosterone did not increase [(35)S]-GTP-γS binding to membranes of HEK-GPER-1 cells, indicating that it is not involved in G protein signaling mediated through GPER-1. During the secretory phases of the estrus cycle, GPER-1 is upregulated on cortical epithelia and localized to the basolateral surface during proestrus and redistributed intracellularly during estrus. GPER-1 is down-modulated during luteal phases of the estrus cycle with significantly less receptor on the surface of renal epithelia. Our results demonstrate that GPER-1 is associated with specific estrogen binding and not aldosterone binding and that GPER-1 expression is modulated during the estrus cycle which may suggest a physiological role for GPER-1 in the kidney during reproduction.

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The incidence of falls fell from 53 in 2011 to 29 in 2012, and there were no fall-related proximal femoral fractures for 3 years after the introduction of NY-mode diuretic therapy. We also found statistically significant differences in muscle and intracellular water volumes in our elderly participants: those with higher care requirements or lower levels of independence had lower muscle or water volumes.

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This article examines the emerging role of the heart failure nurse and the responsibilities and educational and training requirements surrounding such a role. There may be variations in the role and its responsibilities in different health care settings. However the principles are similar and include: history taking, carrying out clinical assessment and making appropriate decisions about patient management within the context of practice. An example of this is nurse supervision of adjusting and titration of medication in a clinic setting or in the patient's own home. A major challenge to this role is defining the limitations and scope of practice. Patients with chronic heart failure (CHF) are generally a frail, elderly population, and often have significant other co-morbidities. They can be on multiple medications and are frequently prescribed sub-optimal doses of evidence-based medication. Many patients are not managed by specialists, thus creating a huge potential for improved management.

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Transient prepubertal exposure to ARB or MR-ant, but not vasodilator, confers protection against the later development of diabetic nephropathy and involves blood pressure-independent protective mechanisms.

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aldactone overdose 2017-03-25

Despite ample data from randomized clinical trials (RCTs), the management of advanced heart failure Actos Cost (HF) varies greatly. We examined the most common refractory questions arising in routine inpatient management of advanced HF.

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Insulin sensitizers, including metformin and thiazolidinediones (TZDs), improve hyperinsulinemia and reproductive dysfunctions Ziac 10 Mg in some women with hyperandrogenism. The extent to which these agents improve hirsutism remains unclear.

aldactone pill identification 2016-08-01

According to American Heart Association/American College of Cardiology Practice Guidelines, electrolyte abnormalities, including abnormal serum potassium concentrations, are considered a correctable cause of a life-threatening ventricular arrhythmia. Ventricular defibrillator Hytrin Drug Class therapy in this situation is a class III indication, and thought to be ineffective and perhaps harmful, although there are minimal data to support this recommendation. The steady-state serum potassium concentration frequently changes during a cardiac arrest. Additionally, the vast majority of cardiac arrest patients have structural heart disease and are commonly treated with a variety of medications that can alter the serum potassium concentration. In the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial, patients with a correctable cause of an electrolyte imbalance were excluded from study participation but were followed in the AVID registry. Similar outcomes were observed among patients in the AVID registry and the main trial. Spironolactone therapy in patients with congestive heart failure decreases all-cause mortality and sudden and nonsudden cardiac death. In a preliminary study of 169 patients with an episode of a sustained ventricular arrhythmia treated with an implantable defibrillator, freedom from appropriate defibrillator therapy was 18% after five years. The probability of appropriate defibrillator therapy was independent of the initial serum potassium concentration. For these reasons, our current clinical practice is to use an implantable defibrillator to treat an initial episode of sustained ventricular tachycardia or ventricular fibrillation that occurs in a patient with structural heart disease and an abnormal serum potassium concentration.

aldactone normal dosage 2017-11-02

NASPAG membership (N = 326; Buy Glucotrol Respondents = 127 (39%))

aldactone 100mg tablet 2016-10-21

Although drug eruptions resembling graft-versus-host disease are rare, GvH-like reactions to the sulfhydryl group of drugs (penicillamine Valtrex Cost , captopril, gold sodium), phenobarbital and hepatitis vaccine have been described. Clinical reports concerning acute GvH-like drug rash are very uncommon and restricted to acetylsalicylic acid and spironolactone. We report on a patient who developed an acute GvH-like drug reaction caused by allopurinol. To our knowledge this variant of cytotoxic drug eruption has not yet been reported in literature.

aldactone tablets 2015-09-30

The hypothalamic-pituitary-adrenocortical system is a complex negative feed-back control mechanism. Under non-stress conditions it functions to maintain a circadian rhythm of adrenal steroid production which is secondary to a circadian fluctuation in the sensitivity to suppression of acth by hydrocortisone. Any stressful stimulus causes an augmentation of steroid production which is due in part to a decrease in sensitivity of acth to suppression. Aldosterone production is not primarily controlled by acth. The increased understanding of this system and of its pathologic alterations has led to the development of a number of pharmacologic techniques which have proved most valuable in evaluating its integrity. Hypothalamic-pituitary function can be assessed by Purchase Viagra the response to the administration of dexamethasone, methopyrapone, bacterial pyrogen and vasopressin. Adrenal cortical function can be assessed by the response to acth, dexamethasone and spironolactone.

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Aldosterone contributes to Biaxin Medication Interactions autonomic dysfunction and intrarenal injury in 2K1C, these effects are mediated by the CNS.

aldactone generic name 2016-09-06

Diuretic agents influence the renal handling of magnesium, causing increased losses of the ion. Continuing magnesium losses may, in the long term, result in a magnesium deficiency. 296 patients with congestive heart failure or arterial hypertension receiving long term diuretic therapy were studied by skeletal muscle biopsies to assess their magnesium status. 65% of the congestive heart failure patients and 42% of the patients with arterial hypertension were Aggrenox Online found to have subnormal values for skeletal muscle magnesium. Studies with the potassium-sparing diuretics amiloride, spironolactone and triamterene demonstrate that these drugs significantly increase the muscle magnesium content in patients on long term diuretic treatment for congestive heart failure and/or arterial hypertension--in addition to their well known positive effect on potassium balance.

aldactone drug interactions 2017-05-31

Heart failure (HF) is a common cause of hospitalisation in most countries. Data on acute precipitants of HF and hospitalisation is not available in Sri Lanka.

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The present authors will add minoxidil to their normal treatment paradigm based on this later study. The previous reasons for it was the quality of the hair produced (generally much shorter than other head hair). For alopecia related to inflammation, the present authors may have discovered a novel therapy--dextroamphetamine sulfate.

aldactone drug class 2015-05-29

The rapid (2 min) nongenomic effects of aldosterone (ALDO) and/or spironolactone (MR antagonist), RU 486 (GR antagonist), atrial natriuretic peptide (ANP) and dimethyl-BAPTA (BAPTA) on the intracellular pH recovery rate (pHirr) via NHE1 (basolateral Na⁺/H⁺ exchanger isoform), after the acid load induced by NH₄Cl, and on the cytosolic free calcium concentration ([Ca²⁺](i)) were investigated in the proximal S3 segment isolated from rats, by the probes BCECF-AM and FLUO-4-AM, respectively. The basal pHi was 7.15±0.008 and the basal pHirr was 0.195±0.012 pH units/min (number of tubules/number of tubular areas=16/96). Our results confirmed the rapid biphasic effect of ALDO on NHE1: ALDO (10⁻¹² M) increases the pHirr to approximately 59% of control value, and ALDO (10⁻⁶ M) decreases it to approximately 49%. Spironolactone did not change these effects, but RU 486 inhibited the stimulatory effect and maintained the inhibitory effect. ANP (10⁻⁶ M) or BAPTA (5×10⁻⁵ M) alone had no significant effect on NHE1 but prevented both effects of ALDO on this exchanger. The basal [Ca²⁺](i) was 104±3 nM (15), and ALDO (10⁻¹² or 10⁻⁶ M) increased the basal [Ca²⁺](i) to approximately 50% or 124%, respectively. RU 486, ANP and BAPTA decreased the [Ca²⁺](i) and inhibited the stimulatory effect of both doses of ALDO. The results suggest the involvement of GR on the nongenomic effects of ALDO and indicate a pHirr-regulating role for [Ca²⁺](i) that is mediated by NHE1, stimulated/impaired by ALDO, and affected by ANP or BAPTA with ALDO. The observed nongenomic hormonal interaction in the S3 segment may represent a rapid and physiologically relevant regulatory mechanism in the intact animal under conditions of volume alterations.

aldactone medicine uses 2015-05-27

Separation, culture and identification of primary hepatic stellate cells (HSCs): The fluids and digestives used in the present study were able to completely remove blood cells, digest hepatocytes and matrix, and effectively separate HSCs. The in situ perfusion was performed at 2 steps: in situ perfusion with pre-perfusion fluid and ex vivo perfusion with enzyme-containing perfusion fluid. Influence of Ald on PAI-1 and Smad expressions in HSCs: cells were divided into control group, Ald group (10(-6) M), spironolactone (SPI) group and Ald+SPI group, and the mRNA and protein expressions of PAI-1 and Smad were detected. Ald induced type I collagen expression in HSCs: Immunohistochemistry was performed to detect type I collagen expression in the supernatant of control group, Ald group (10(-6) M), TGF-β1 group, and Ald+TGF-β1 group. Influence of Ald and TGF-β1 on PAI-1 expression in HSCs: cells were divided into control group, Ald group (10(-6) M), TGF-β1 group, and Ald+TGF-β1 group, and the mRNA and protein expressions of PAI-1 were determined by RT-PCR and Western blot assay, respectively. Synergistic effect of Ald and TGF-β1 on PAI-1 expression in HSCs: cells were divided into control group, Ald group (10(-6)), TGF-β1 group, Ald (10(-6) M)+TGF-β1 group, Ald (10(-7) M)+TGF-β1 group and Ald (10(-8) M)+TGF-β1 group, and the mRNA and protein expressions of PAI-1 were detected by RT-PCR and Western blot assay, respectively.

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We included into this study 100 patients with hypertensive disease (HD) or ischemic heart disease (IHD) and FC III CHF with compromised systolic left ventricular (LV) function. All patients were randomized into two groups. In addition to complex background therapy (quinapril, torasemide, spironolactone) patients of group 1 (n=56, age 57.5+/-21.7 years) were given metoprolol succinate (59.1+/-12.1 mg/day) and patients of group 2 (n=44, age 57.1+/-21.4 years) - ivabradine (12.1+/-4.6 mg/day). Examination at baseline and after 6 months included cardiorespiratory synchronism test (in order to quantitatively define RAS), echocardiography, treadmill test, six minute walk test. Cardiovascular complications (CVC) were registered during 12 months of study treatment.