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PubMed2001

Indapamide, a thiazide-like diuretic, decreases bone resorption in vitro.

We recently showed that indapamide (IDP), a thiazide-related diuretic, increases bone mass and decreases bone resorption in spontaneously hypertensive rats supplemented with sodium. In the present study, we evaluated the in vitro effects of this diuretic on bone cells, as well as those of hydrochlorothiazide (HCTZ), the reference thiazide, and acetazolamide (AZ), a carbonic anhydrase (CA) inhibitor. We showed that 10(-4) M IDP and 10(-4) M AZ, as well as 10(-5) M pamidronate (APD), decreased bone resorption in organ cultures and in cocultures of osteoblast-like cells and bone marrow cells in the presence of 10(-8) M 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]. We investigated the mechanism of this antiresorptive effect of IDP; IDP decreased osteoclast differentiation as the number of osteoclasts developing in coculture of marrow and osteoblast-like cells was decreased markedly. We then investigated whether IDP affected osteoblast-like cells because these cells are involved in the osteoclast differentiation. Indeed, IDP increased osteoblast-like cell proliferation and alkaline phosphatase (ALP) expression. Nevertheless, it did not modify the colony-stimulating factor 1 (CSF-1) production by these cells. In addition, osteoblast-like cells expressed the Na+/Cl- cotransporter that is necessary for the renal action of thiazide diuretics, but IDP inhibited bone resorption in mice lacking this cotransporter, so the inhibition of bone resorption and osteoclast differentiation did not involve this pathway. Thus, we hypothesized that IDP may act directly on cells of the osteoclast lineage. We observed that resorption pits produced by spleen cells cultured in the presence of soluble osteoclast differentiation factor (sODF) and CSF-1 were decreased by 10(-4) M IDP as well as 10(-5) M APD. In conclusion, in vitro IDP increased osteoblast proliferation and decreased bone resorption at least in part by decreasing osteoclast differentiation via a direct effect on hematopoietic precursors.

Animals↗
PubMed2005

Expiratory flow limitation is associated with orthopnea and reversed by vasodilators and diuretics in left heart failure.

BACKGROUND: In patients with acute left heart failure (LHF), orthopnea has also been related to the occurrence or worsening of expiratory flow limitation (EFL) in the supine position. We wished to assess whether short-term treatment with vasodilators and diuretics was able to abolish supine EFL and whether this could help to control orthopnea in patients with acute LHF. METHODS: In nine nonobese (ie, mean [+/- SD] body mass index, 24 +/- 5 kg/m2), never-smoker patients (two men and seven women; mean age, 77 +/- 7 years) with acute LHF (mean ejection fraction, 43 +/- 15%), we assessed EFL by the negative expiratory pressure method and dyspnea by the Borg scale, with patients in both the seated and supine positions, before and after short-term treatment with vasodilators and diuretics until hospital discharge. Orthopnea was defined as a positive difference in the Borg score between measurements made with the patient in the supine and seated positions. Postural variations in the end-expiratory lung volume were inferred from changes in inspiratory capacity (IC) that were measured under the same circumstances. RESULTS: Before treatment, with the patient in the seated position the mean dyspnea score was 1.5 +/- 0.5, the mean IC was 1.49 +/- 0.38 L, seven patients were non-flow-limited, and two patients were flow-limited. During recumbency, the mean dyspnea score was 2.7 +/- 0.5 (p < 0.01 vs seated position values), the mean IC was 1.66 +/- 0.45 L, and seven patients exhibited EFL. After a mean duration of 17 +/- 8 days of treatment (range, 7 to 28 days), EFL was detected in two patients only in the supine position, IC increased both in the seated position (1.65 +/- 0.34 L; p < 0.01) and the supine position (1.81 +/- 0.41 L; p = 0.07) position, and, although only two patients denied orthopnea, the mean dyspnea score during recumbency actually decreased to 1.9 +/- 1.0 (p < 0.05). CONCLUSIONS: Our results indicate that short-term treatment with vasodilators and diuretics is able to control orthopnea and to remove supine EFL in most patients with acute LHF, suggesting a posture-related increase in bronchial obstruction as the main mechanism of EFL, which appears to play a role in the occurrence and severity of orthopnea in these circumstances.

Aged↗
PubMed1997

Long-term evaluation of combined antihypertensive therapy with lisinopril and a thiazide diuretic in patients with essential hypertension.

For the treatment of hypertension, the combination of an angiotensin-converting enzyme (ACE) inhibitor and a thiazide diuretic is supported by multiple lines of evidence, because these drugs have synergistic action and are expected to cancel out each other's adverse side effects. However, the long-term outcome of this combination antihypertensive therapy is not entirely clear. In the present multicenter open trial, we investigated the long-term efficacy and safety of combined antihypertensive therapy with an ACE inhibitor, lisinopril, and a thiazide diuretic, trichlormethiazide. A total of 466 patients with essential hypertension were treated with lisinopril alone (monotherapy group, n = 360) or with a combination of lisinopril with trichlormethiazide (combination therapy group, n = 106) for 1 year. The average blood pressure was effectively lowered to below 150/90 mmHg in both the monotherapy and the combination therapy groups throughout the study period. The average maintenance dose of lisinopril was lower when combined with thiazide than when given alone (9.8 vs. 11.5 mg/day, p < 0.001). Dry cough was the major side effect of lisinopril; no severe adverse effects were observed. The incidence of cough was not significantly different between the monotherapy group (13.1%) and the combination therapy group (11.3%). The increase in serum potassium observed in the monotherapy group was reversed by the concurrent use of the thiazide diuretic in the combination therapy group. Fasting blood glucose was significantly reduced in the monotherapy group; the reduction observed in the combination therapy group was not significant. Thus, the present results provide useful information as to the effectiveness and safety of combined antihypertensive therapy with lisinopril and a thiazide in comparison with monotherapy with lisinopril.

Adult↗
PubMed2003

Combination therapy with ACE inhibitors/angiotensin II receptor antagonists and diuretics in hypertension.

Essential hypertension is a very heterogeneous disease and different pressor mechanisms might interact to increase blood pressure. It is therefore not surprising that antihypertensive drugs, given as monotherapy, normalize blood pressure in only a fraction of hypertensive patients. This is, for instance, the case for diuretics, angiotensin converting enzyme (ACE) inhibitors and angiotensin II (AT1) receptor antagonists administered as single agents. The rationale for combining antihypertensive agents relates in part to the concept that the blood pressure-lowering effect may be enhanced when two classes are coadministered. Also, combination therapy serves to counteract counter-regulatory mechanisms that are triggered whenever pharmacologic intervention is initiated and that act to limit the efficacy of the antihypertensive medication. For example, the compensatory rise in renin secretion induced by sodium depletion may become the predominant factor sustaining high blood pressure. Simultaneous blockade of the renin-angiotensin system, with either an ACE inhibitor or an AT1-receptor blocker, makes this compensatory hyper-reninemia ineffective and allows maximum benefit from sodium depletion. The combination of a blocker of the renin-angiotensin system and a low dose of a diuretic increases the effectiveness, but not at the expense of tolerability compared with the individual components administered alone. Fixed-dose combinations containing an ACE inhibitor or an AT1-receptor blocker and a diuretic are therefore likely to become increasingly used not only as second-line therapy but also as first-line treatment.

Angiotensin Receptor Antagonists↗
PubMed1992

The diuretic effect of calcium entry blockade in normals and hypertensive patients.

Calcium entry blockers have been shown to exert hemodynamic and diuretic effects in the kidney. The diuretic effects can be demonstrated most clearly in the isolated perfused kidney, not influenced by compensatory mechanisms such as a lower blood pressure or changes of hormones. However, they can also be shown in vivo in humans. We studied the renal effects of calcium entry blockade after the first dosage and after continued oral dosages of 20 mg nicardipine tid in patients with essential hypertension and in normotensive controls. Renal function was determined during maximal free water clearance, allowing estimation of changes in "proximal" and "distal" tubular sodium reabsorption. Results showed a natriuretic effect. In the control subjects, clearance results were compatible with a decrease of proximal and distal tubular reabsorption, but in the hypertensive group natriuresis was mainly achieved by an increase of the glomerular filtration rate and a decrease of fractional distal reabsorption. In both groups the natriuresis occurred concomitantly with a lower blood pressure. The ratio plasma renin activity/plasma aldosterone concentration increased, although nicardipine did not inhibit the increase of plasma aldosterone during angiotensin II infusion. Pre-treatment with the calcium entry blocker nitrendipine enhanced the natriuretic effect of atrial natriuretic factor (ANF) in sodium replete normal volunteers. Facilitation of sodium excretion by human ANF may be an additional diuretic mechanism of calcium entry blockers.

Calcium Channel Blockers↗
PubMed1985

Long term experience of felodipine in combination with beta-blockade and diuretics in refractory hypertension.

Felodipine, a new dihydropyridine, was given to 58 hypertensive patients in combination with an adrenergic beta-receptor antagonist and a diuretic agent. In all but 2 patients the blood pressure was unsatisfactorily controlled on standard triple therapy, i.e. alpha beta-blocker, a diuretic and a vasodilator. A 48-week follow-up was completed by 54 patients. After an initial dose titration period, the maintenance dose of felodipine was 5 mg twice daily in 14 patients and 10 mg twice daily in 34 patients. In the remaining 6 patients, the dose ranged from 5 mg every morning to 25 mg twice daily. The dosages of beta-blocking agent and diuretic were considerably reduced during the study period. Mean supine blood pressure was reduced from 170/101 mm Hg on triple therapy before felodipine to 145/86 mm Hg (p less than 0.001) after 2 weeks on felodipine. This improvement was sustained throughout the study and was measured at 144/86 mm Hg (p less than 0.001) after 48 weeks. There was no increase in resting heart rate and no orthostatic fall in blood pressure. Bodyweight was not increased and felodipine was generally well tolerated. Three patients were withdrawn owing to side effects and 1 was socially non-compliant. It is concluded that felodipine is a potent and well tolerated vasodilator, and will be useful in the long term combination treatment of previously refractory hypertension.

Adrenergic beta-Antagonists↗
PubMed1985

Interactions of NSAIDs with diuretics and beta-blockers mechanisms and clinical implications.

Indomethacin attenuates the antihypertensive effect of both thiazide diuretics and beta-adrenoceptor blocking drugs. The mechanisms of these interactions are poorly understood but sodium and water retention, suppression of plasma renin activity, alterations in adrenoceptor sensitivity and impaired synthesis of vasodilator prostaglandins may all contribute to this effect. Other non-steroidal anti-inflammatory drugs (NSAIDs) may share this property of indomethacin but sulindac, which is a selective inhibitor of extrarenal prostaglandin synthesis, appears not to. This may have important clinical and theoretical implications. Clinicians must beware of this potential interaction in any patient receiving treatment for hypertension. NSAIDs may also inhibit the natriuretic response to diuretics with resultant adverse effects in patients with heart failure and other forms of oedema. NSAIDs may also have adverse nephrotoxic effects which may be exacerbated by diuretic therapy.

Adrenergic beta-Antagonists↗
PubMed1986

Diuretics in cardiac oedema.

Cardiogenic oedema results from an increase in capillary hydrostatic pressure (either pulmonary or systemic). This increase produces a reduction in the plasma colloidosmotic pressure-capillary pressure gradient, facilitating the accumulation of fluid in the interstitial space and reducing the circulating plasmatic volume. The administration of diuretics to patients with acute ventricular dysfunction has both haemodynamic and renal effects, and causes a reduction in extravascular fluid. In chronic heart failure, the use of diuretics may result in a haemodynamic improvement once the volaemia is reduced. However, in some patients diuretics may cause activation of the neurohumoral axis and consequently a transient haemodynamic deterioration.

Diuretics↗
PubMed1986

Diuretics, potassium and arrhythmias in hypertensive coronary disease.

It has been proposed that modest changes in plasma potassium can alter the tendency towards cardiac arrhythmias. If this were so, patients with coronary artery disease might be especially susceptible. Thus, myocardial electrical excitability was measured in patients with mild essential hypertension and known coronary artery disease after 8 weeks of treatment with a potassium-conserving diuretic (amiloride) and a similar period on a potassium-losing diuretic (chlorthalidone) in a randomised study. Plasma potassium concentrations were on average 1 mmol/L lower during the chlorthalidone phase compared to amiloride therapy. Blood pressure and volume states as assessed by bodyweight, plasma renin and noradrenaline (norepinephrine) concentrations were similar on the 2 regimens. Compared to amiloride treatment, the chlorthalidone phase was associated with an increased frequency of ventricular ectopic beats (24-hour Holter monitoring) and a higher Lown grading, increased upslope and duration of the monophasic action potential, prolonged ventricular effective refractory period, and increased electrical instability during programmed ventricular stimulation. The above results indicate that because potassium-losing diuretic therapy can increase myocardial electrical excitability in patients with ischaemic heart disease, even minor falls in plasma potassium concentrations are probably best avoided in such patients.

Chlorthalidone↗
PubMed1986

Diuretic therapy in congestive heart failure for the elderly patient.

The incidence of congestive heart failure (CHF) in the elderly increases with age as 80% of patients hospitalised with CHF are older than 60 years of age. In this age group CHF may result from several factors such as coronary artery disease, hypertension, valvular disease or intrinsic myocardiopathies. Important alterations of renal physiology have been observed in this condition: decreases in renal plasma flow and glomerular filtration rate, and increases in renal venous pressure. Natriuretic hormone inhibition occurs and renin-angiotensin-aldosterone system activation and antidiuretic hormone secretion increase, resulting in positive water and sodium balances that contribute to the manifestations of congestive heart failure. The treatment of CHF in the elderly is similar to that in younger patients; the difference in management is determined by the severity of the disease and the side effects of the drugs used. Diuretics increase water and sodium elimination by the kidney and increase the systolic volume of the left ventricle, probably by the reduction of preload and afterload. Diuretic therapy must be pursued carefully in patients receiving digitalis, especially in those elderly individuals who may be on restricted diets: the most common adverse effects of diuretics in this age group are hypovolaemia, hyponatraemia, hypokalaemia and hypomagnesaemia.

Aged↗
PubMed1986

Diuretic therapy for hypertension in the elderly.

Recent studies have confirmed the benefits of treating hypertension in the elderly. Thiazide diuretics appear to be effective in achieving goal blood pressure in a majority of patients above the age of 60 years. Increasing concern regarding the biochemical abnormalities associated with diuretic therapy has led to the more widespread use of lower doses of these agents. Preliminary results from a study of hydrochlorothiazide +/- amiloride treatment in 99 hypertensive patients aged 65 to 80 years indicate that hydrochlorothiazide 25 to 50 mg/day will lower diastolic blood pressure to less than 90 mmHg in about 90% of elderly patients with mild to moderate elevations in blood pressure. These lower dosages of hydrochlorothiazide were only occasionally associated with mild hypokalaemia. However, the addition of amiloride to the treatment regimen resulted in the maintenance of normal serum potassium concentrations. Thus, relatively low doses of thiazide diuretics may effectively lower blood pressure in elderly hypertensive patients while causing fewer biochemical abnormalities than previously associated with the use of these drugs.

Aged↗
PubMed1986

Guidelines for rational diuretic use in the elderly.

The elderly not only have lower body stores of potassium, but also tend to eat a diet relatively low in potassium content. Loss of muscle strength, constipation and mental apathy are all features of potassium deficiency. In addition, serious arrhythmias have been attributed to hypokalaemia and must therefore be prevented. While potassium supplements may replete body potassium stores, they often require large amounts and may still be ineffective in preventing diuretic-induced hypokalaemia. Thus, several guidelines for the rational and safe use of diuretics in the elderly have been proposed including in addition to potassium supplementation, the determination of dietary and total body potassium sources, dosage of the diuretic and intensity of the diuresis, and the relationship between potassium and calcium and magnesium.

Aged↗
PubMed1991

The loop diuretic torasemide in chronic renal failure. Pharmacokinetics and pharmacodynamics.

The pharmacodynamic effect of a diuretic agent is essentially dependent on its renal elimination characteristics. The influence of renal function on the pharmacodynamic and pharmacokinetic characteristics of a diuretic should therefore be considered. The results of a study with torasemide given intravenously in healthy subjects and in patients with stable chronic renal failure of various degrees are reported and discussed. After a single dose of torasemide 20mg, a marked diuresis was observed and electrolyte excretion was increased, whereas the glomerular filtration rate was unchanged. Throughout the duration of action (tau) of torasemide, drug-induced excretion of Cl-, Na+, K+, Ca++ and Mg++ was linearly related to the creatinine clearance (CLcr), and excretion of K+ and Ca++ were closely related to that of Na+ over the entire range of CLcr. Similarly, excretion of Mg++ was related to that of K+. As occurs with furosemide (frusemide), torasemide induced a kaliuresis which amounted to 12% of natriuresis. This kaliuretic effect of loop diuretics is less than that of thiazides. Beyond tau, e.g. over a 24-hour period, kaliuresis was no longer correlated with natriuresis. The extent to which a rebound effect occurred was diminished with increasing renal impairment. tau averaged 6 hours and was independent of CLcr. The mean half-life (t1/2) of torasemide was approximately 5 hours and was independent of renal function, since renal clearance accounted for only around 25% of total body clearance. In contrast to the parent drug, however, the active minor metabolite M1 and the inactive main metabolite, M5, were found to accumulate in patients with chronic renal failure.

Animals↗
PubMedDate not supplied

Reduction of the endocochlear potential by the new "loop" diuretic, bumetanide.

The effect of bumetanide upon the endocochlear potential (EP) was examined in 46 guinea pigs. The EP was reduced with dosages of 5 mg/kg or more. The maximum depression of the EP (reduction to -30 to -40 mV) was obtained at a dosage of 30 mg/kg. The recovery of the potential was incomplete at any dosage within three hours and the response pattern of the EP to bumetanide was similar to that to ethacrynic acid. The present experiments revealed that bumetanide, by weight, has a stronger ototoxic potency than the other "loop" diuretics--furosemide and ethacrynic acid. However, the diuretic effect of 1 mg bumetanide is equivalent to 40 to 60 mg furosemide or ethacrynic acid. Therefore, the relative ototoxic potency of bumetanide is much smaller suggesting that from a clinical standpoint bumetanide is much safer than the other "loop" diuretics.

Action Potentials↗
PubMed1987

Ultrafiltration in diuretic-resistant cardiac failure.

Ultrafiltration was performed in 13 patients with diuretic-resistant cardiac failure. All patients had severely distressing peripheral edema and ultrafiltration was successfully completed in 12 patients, all of whom sustained symptomatic improvement. The volume of fluid removed ranged from 3.7 to 23 L, mean 11.8 L. Weight reduction produced by ultrafiltration continued over the following week, indicating an improved response to diuretic therapy. Ultrafiltration is an effective therapeutic intervention in the management of a small but well-defined group of patients with diuretic-resistant cardiac failure.

Aged↗
PubMed1994

Diuretics in acute renal failure.

Studies on the ability of loop diuretics, mannitol, dopamine, and atrial natriuretic peptide to ameliorate or reverse human acute renal failure are reviewed. A precise role for diuretic therapy in this clinical setting has not been established. Most reports are retrospective, poorly controlled, or simply anecdotal. There is a need for prospective, randomly allocated studies on adequate numbers of patients. While the use of diuretic agents may improve fluid balance management in patients at risk of developing acute renal failure, maintenance of adequate effective circulating volume and oxygen delivery probably provides the best-proven protection.

Acute Kidney Injury↗
PubMed1983

Studies on the renal receptors of loop diuretics.

The principal renal action of loop diuretics is to inhibit active NaCl transport in the thick ascending limb of the loop of Henle. However, apart from their specific tubular action, kidney function may be affected in other ways. By employing the enantiomeres of the new loop diuretic ozolinone, non-stereospecific increase in renal blood flow and inhibition of tubular secretion of p-aminohippurate and urate were found. In contrast, electrolyte transport in the loop of Henle was inhibited stereospecifically. Perfusion of single loops of rat kidneys in vivo with sugar-specific lectins suggested that a fucose-containing glycoprotein is involved in electrolyte transport in this tubular segment. Loop diuretics might interact with this glycoprotein, leading to inhibition of electrolyte transport. Evidence is presented to suggest that this protein is the Tamm-Horsfall protein. This fucose-containing glycoprotein is localized in the cell membranes of the thick ascending limb of the loop of Henle. It binds furosemide at concentrations very close to those required for inhibition of electrolyte transport in vivo. Furthermore, there is complete agreement between the sodium concentration necessary for stimulation of active transport in isolated thick ascending limbs of the loop of Henle and that necessary for binding of furosemide to the Tamm-Horsfall glycoprotein.

Animals↗
PubMed1989

Beta-blockers and diuretics. The HAPPHY and MAPHY studies.

The question whether initial antihypertensive treatment with a beta-blocker prevents hypertensive complications better than initial treatment with a non-betablocker, mainly diuretic based treatment, has been studied in recent large-scale studies like the Medical Research Council (MRC) trial, the International Prospective Primary Prevention Study in Hypertension (IPPPSH), the Heart Attack Primary Prevention in Hypertension (HAPPHY) study and the Metoprolol Atherosclerosis Prevention in Hypertensives (MAPHY) study. The first three studies were unable to find a more beneficial effect of beta-blockers than of thiazide diuretics. The MAPHY study, however, found a lower total mortality, in the metoprolol treated group than in the diuretic treated. As the HAPPHY and MAPHY studies share a substantial part of patient-years and number of deaths, these diverging results have evoked confusion and debate. This paper presents the main results of both studies and discusses the possible reasons for the different outcome.

Adrenergic beta-Antagonists↗