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PubMed1978

The relation between extra- and intracellular electrolytes in patients with hypokalemia and/or diuretic treatment.

The relation between extra- and intracellular electrolytes has been studied by means of percutaneous muscle biopsies in 107 patients with hypokalemia and/or treatment with diuretics. No relation was found between the extra- and intracellular concentrations of Na or Mg. The serum and muscle contents of K correlated weakly. The correlation coefficient tended to be stronger when S-creatinine was normal, total carbonate was between 25 and 30 mmol/l, muscle Mg content was greater than or equal to 3.95 mmol/100 g fat free dry solids, and when no treatment was given with digitalis and/or diuretics.

Aged↗
PubMed1980

Urinary zinc excretion during treatment with different diuretics.

Urinary zinc excretion was studied in a randomized trial in 9 patients during treatment with bendroflumethiazide, chlorthalidone and hydrochlorothiazide and in another 9 patients during treatment with bumetanide, furosemide and triamterene. During treatment with the thiazides, the zinc concentration rose by 30% and the total amount of zinc excretion increased by 60%. In contrast, during treatment with the loop-diuretics, urine zinc concentration diminished and the total amount of zinc excretion increased much less than during therapy with the thiazides. With respect to the importance of zinc as an essential element in human metabolism and the frequency of diuretic treatment, the observed increased urinary losses of zinc deserve further attention.

Adult↗
PubMed1981

Thiazide diuretics, hypokalemia and cardiac arrhythmias.

Thiazide diuretics are widely accepted as the cornerstone of antihypertensive treatment programs. Hypokalemia is a commonly encountered metabolic consequence of chronic thiazide therapy. We treated 38 patients (22 low renin, 16 normal renin) with moderate diastolic hypertension with hydrochlorothiazide (HCTC) administered on a twice daily schedule. Initial dose was 50 mg and the dose was increased at monthly intervals to 100 mg, 150 mg and 200 mg daily until blood pressure normalized. The serum K during the control period was 4.5 +/- 0.2 mEq/l an on 50, 100, 150 and 200 mg HCTZ daily 3.9 +/- 0.3, 3.4 +/- 0.2, 2.9 +/- 0.2, and 2.4 +/- 0.3 mEq/l, respectively. Corresponding figures for whole body K were 4107 +/- 208, 3722 +/- 319, 3628 +/- 257, 3551 +/- 336, and 3269 +/- 380 mEq, respectively. In 13 patients we observed the effects of HCTZ therapy (100 mg daily) on the occurrence of PVC's during rest as well as during static and dynamic exercise. During rest we observed 0.6 +/- 0.08 PVC beats/min +/- SEM and during static and dynamic exercise 0.6 +/- 0.06 and 0.8 +/- 0.15, respectively. Corresponding figures during HCTZ therapy 100 mg daily were 1.4 +/- 0.1, 3.6 +/- 0.7 and 5.7 4/- 0.8, respectively. The occurrence of PVC's correlated significantly with the fall in serum K+ observed r = 0.72, p less than 0.001. In conclusion we found that thiazide diuretics cause hypokalemia and depletion of body potassium. The more profound hypokalemia, the greater the propensity for the occurrence of PVC's.

Adult↗
PubMed1981

The effect of diuretics on lymphocyte magnesium and potassium.

Lymphocytes have advantages over other tissues, such as erythrocytes and muscle, for assessing intracellular magnesium and potassium. During experimental magnesium deficiency in rats, the magnitude of the magnesium loss from lymphocytes was similar to that of cardiac and skeletal muscle. During experimental potassium deficiency, cardiac muscle retained potassium more effectively than skeletal muscle. The magnitude of the potassium loss from lymphocytes was of similar magnitude to that of cardiac muscle. Chronic congestive heart failure patients being treated with the loop-blocking diuretic, furosemide, were found to have significantly reduced lymphocyte magnesium (p less than 0.05) and potassium (p less than 0.01) compared to values obtained in 20 control subjects. The effects of acute administration of the potassium-sparing diuretic, amiloride, were investigated in 10 congestive heart failure patients. Each patient was studied over a 6-day period comprising a 3-day control period involving furosemide administration, followed immediately by a 3-day test period when amiloride (10 mg twice daily) was added to the therapeutic regimen. Amiloride reduced urinary potassium and magnesium, and increased both plasma and lymphocyte potassium and magnesium. Under these conditions, amiloride exerted magnesium-sparing actions in addition to its well-established potassium-sparing actions. The magnesium-sparing actions may be beneficial in that many experimental studies have shown that magnesium is required for maintenance and restoration of cell potassium.

Aged↗
PubMed1978

Effect of diuretic, beta-adrenoceptor blocking agent and their combination on elevated blood pressure and serum potassium: a cross-over study.

1. The antihypertensive effect of a new beta-adrenoceptor blocking agent, trimepranol (10--14 mg/twice daily), chlorthalidone (50 mg every second day) and their combination was studied in eighteen patients with mild to moderate essential hypertension. In a controlled randomized cross-over study the drugs were given for 6 week periods. 2. A significant and equal decrease in blood pressure was achieved both with trimepranol and chlorthalidone, whereas their combination was significantly more effective. 3. Trimepranol significantly antagonized the chlorthalidone-induced hypokalemia. 4. The results favor the use of diuretic or diuretic-beta-adrenoceptor blocker combination over beta-adrenoceptor blocker monotherapy in the treatment of mild to moderate hypertension.

Adrenergic beta-Antagonists↗
PubMed1979

Diuretics as initial treatment for essential hypertension.

1 In the United States, the thiazide diuretics are considered the cornerstone of all antihypertensive regimens for four reasons: by themselves, they are capable of controlling the blood pressure in 60-70% of the hypertensive population; they prevent the sodium retention produced by all other antihypertensive agents; they can be given once a day; and they are inexpensive. 2 Despite these advantages, the thiazide do cause hypokalaemia hyperuricaemia and hyperglycaemia. The incidence of hypokalaemia (K less than 3.0 mEq/l) is only 2-4%; the incidence of hyperuricaemia (uric acid greater than 10 mg per cent is 3-4%; and the incidence of hyperglycaemia is 1-2%. 3 The possibility that a beta-blocking agent combined with a thiazide diuretic might produce better BP control, prevent thiazide-induced abnormalities and exert a coronary prevention action with once daily administration would suggest that such a combination should be the ideal initial therapy for most patients with hypertension.

Adrenergic beta-Antagonists↗
PubMed1983

The pharmacokinetics and diuretic effects of piretanide in chronic renal insufficiency.

The pharmacokinetics of piretanide, a new loop diuretic, were studied in four patients with GFR 4.7-14.8 ml/min. An oral dose of piretanide 18 mg was given at 08.00 h in two patients and at 08.00 h and 14.00 h in two. Blood samples were drawn after 0.5, 1, 2, 3, 4, 6, 8, 10, 12 and 24 h. Serum concentrations of piretanide were estimated by radioimmunoassay. The peak serum concentration of piretanide (1-2 h after drug administration) was 510-880 ng/ml, independent of renal function. Elimination half life (t1/2) was 1.2-4.1 h, area under the curves (AUC(0,24)) 1.63-2.44 micrograms ml-1 h, volume of distribution (Vz) 0.30--0.741#kg, total plasma clearance (CL) 122.8-184.0 ml/min and renal clearance (CLR) 1.5-5.2 ml/min. The clinical effects of oral treatment with piretanide 18 mg twice daily were compared with bumetanide 3 mg twice daily in eight patients with renal failure (GFR 2.2-24.5 ml/min). Both drugs equally increased the 24 h output of urine (delta V), sodium (delta UNaV), chloride (delta UC1V), potassium (delta UKV) and calcium (delta UCaV). Fractional excretion of sodium (ENa%) was doubled by piretanide in patients with GFR less than 8 ml/min while a five fold increase was found in patients with GFR greater than 8 ml/min. The onset of effect was the same for both drugs, but the duration exceeded 6 h only for piretanide. Both drugs were most effective on the first of two consecutive treatment days. Delta UC1V was always greater than delta UNaV and urinary phosphate excretion was unchanged, as expected of a loop diuretic without significant proximal effects. Metabolic or clinical side effects were not noticed.

Bumetanide↗
PubMed1987

Comparison of ketanserin and slow-release nifedipine added to the treatment of hypertensive patients uncontrolled by a thiazide diuretic plus beta-adrenoceptor blocker.

1. Ketanserin or slow-release nifedipine were added to the treatment of 24 patients with hypertension uncontrolled by a thiazide diuretic plus beta-adrenoceptor antagonist in an observer-blind, randomised parallel-group study of 6 months duration. 2. At 6 months the mean falls in supine blood pressure were for ketanserin (mean daily dose 77 mg) 7/5 mm Hg and for nifedipine (mean daily dose 62 mg) 27/10 mm Hg. The difference between the treatments was significant for systolic blood pressure (P less than 0.02) and mean arterial pressure (P less than 0.05). Six nifedipine-treated patients reached target blood pressure, compared with one patient with ketanserin (P less than 0.02). 3. One patient taking nifedipine, and none taking ketanserin withdrew because of side-effects. The tolerability of the two drugs was broadly similar. 4. Ketanserin treatment was associated with significant changes in supine pulse rate (-8 beats min-1, P less than 0.05) and corrected QT interval (+27 ms, P less than 0.05). Nifedipine treatment had no effect on these variables. The change in pulse rate was significantly different between the groups. 5. In patients treated with a diuretic and beta-adrenoceptor blocker who required additional treatment ketanserin was significantly inferior to nifedipine.

Adrenergic beta-Antagonists↗
PubMed1991

Analysis of the natriuretic action of a loop diuretic, piretanide, in man.

1. The renal responses to a loop diuretic, piretanide, were investigated in a group of fourteen healthy volunteers. The effect of fluid replacement on the drug-response relationship was evaluated in the absence and in the presence of probenecid pretreatment following both oral and intravenous administration of piretanide. 2. Urinary excretion of piretanide was greater when volume losses were replaced than in the absence of volume replacement (i.v. dose: 3.32 +/- 0.15 vs 2.55 +/- 0.23 mg 6 h-1, P less than 0.01; oral dose: 2.57 +/- 0.09 vs 1.87 +/- 0.27 mg 6 h-1, P less than 0.01). With intravenous piretanide urinary excretion of sodium was likewise greater in the fluid replaced group (198 +/- 4 vs 141 +/- 10 mmol 6 h-1, P less than 0.01); these differences caused by fluid replacement did not however occur after oral dosing of piretanide (181 +/- 12 vs 167 +/- 14 mmol 6 h-1). 3. Probenecid pretreatment significantly decreased the renal excretion of piretanide in all subjects and consistently decreased the natriuretic response with the exception of intravenous piretanide challenge in subjects not undergoing fluid replacement. In this situation, despite probenecid causing a decrease in the amount of drug excreted (2.55 +/- 0.23 vs 1.63 +/- 0.15 mg 6 h-1, P less than 0.05) the sodium output was unaltered (141 +/- 10 vs 152 +/- 16 mmol 6 h-1, NS). 4. Complete replacement of the induced fluid losses resulted in the enhancement of the renal response, without affecting the shape of the diuretic response curve, of either the intravenous or orally administered piretanide.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1993

A comparison of three diuretic regimens in heart failure.

Eight patients with mild heart failure were treated in random order for 1 week with 2 mg bumethanide at 0800 and 1200 (treatment 1) h, 1 mg bumethanide at 0800, 1200, 1800, 2200 (treatment 2) and 5 mg bendroflumethiazide at 0800 and 1800 (treatment 3) h. The 'quality of life' did not differ significantly between the three treatment periods. At the presumed trough of the diuretic effect the circulating blood volume was largest during treatment 1; it was 6.3% smaller during treatment 2 (P < 0.02) and 6.7% lower during treatment 3 (P < 0.05). In comparison with treatment 1, the maximal increase in rate-pressure product during physical exercise was 24.6% higher in treatment 3. Compared with treatment 1 the area under the curve (AUC) for plasma lactate during physical exercise was 14% lower during treatment 2 (P < 0.05) and 18% lower during treatment 3 (P < 0.01). These findings suggest that the type of program for diuretic therapy influences the magnitude of inevitable diurnal fluctuations in body fluids, the ability of the heart to work and the ability of the body to adjust to the oxygen demand.

Aged↗
PubMed1993

Oral magnesium supplementation restores the concentrations of magnesium, potassium and sodium-potassium pumps in skeletal muscle of patients receiving diuretic treatment.

In 76 consecutive patients who had received diuretics for 1-17 years for arterial hypertension or congestive heart failure, muscle concentrations of magnesium, potassium, and sodium-potassium pumps were significantly reduced compared to 31 age- and sex-matched controls. Thirty-six patients with muscle magnesium and/or potassium below the control level received oral magnesium hydroxide supplement for 2-12 weeks (n = 20) or 26 weeks (n = 16). After short-term (2-12 weeks) magnesium supplementation muscle parameters were increased, but far from normalized. After magnesium supplementation for 26 weeks, the muscle concentrations of magnesium, potassium and sodium-potassium pumps were normalized in most cases. Oral magnesium supplementation may restore diuretic-induced disturbances in the concentrations of magnesium, potassium and sodium potassium pumps in skeletal muscle. A supplemental period of at least 6 months seems to be required before complete normalization can be expected.

Administration, Oral↗
PubMed1995

The role of potassium in postural hypotension: electrolytes and neurohumoral factors in elderly hypertensive patients using diuretics.

OBJECTIVE: To study the association between postural hypotension and (i) electrolyte levels and (ii) neurohumoral factors in elderly hypertensive patients using diuretics. DESIGN: Cross-sectional study of patients and controls. SETTING: The subjects were gathered from senior citizen clubs or they were referred to the study by general practitioners. The subjects were examined on a geriatric ward in Turku City Hospital. SUBJECTS: Seven subjects with postural hypotension and 13 controls. MEASUREMENTS: Plasma electrolyte levels and neurohumoral response to head-up tilt. RESULTS: There were significantly more hypokalaemic subjects in the postural hypotension group (5/7) than in the control group (1/13) (P < 0.01). The plasma potassium level was negatively correlated to plasma aldosterone (r = -0.57; P < 0.01) and renin activity (r = -0.69; P < 0.001). Subjects with postural hypotension had higher levels of noradrenaline, both supine (P < 0.05) and during tilt (P < 0.05). There were no significant differences in supine or tilt levels of plasma adrenaline, vasopressin, atrial natriuretic peptide, aldosterone and renin activity between the groups. CONCLUSION: The results suggest that potassium depletion is associated with postural hypotension in elderly hypertensive patients using diuretics. However, it is unclear whether there is a causative link between potassium depletion and postural hypotension or whether they are both caused by some other factor, e.g. volume contraction.

Aged↗
PubMed2005

Effects of long-term treatment with loop diuretics on bone mineral density, calcitropic hormones and bone turnover.

BACKGROUND: Loop diuretics (LD) are widely used in the treatment of cardiovascular diseases and disorders with fluid accumulation. LD are known to increase renal calcium losses and may thereby affect calcium homeostasis and bone metabolism. OBJECTIVE: We studied to what extent long-term treatment with LD affects calcium homeostasis and bone metabolism. DESIGN AND SUBJECTS: In a cross-sectional design we compared 140 postmenopausal women treated with a LD for more than 2 years with 140 age-matched women not in diuretic therapy. RESULTS: Treatment with LD was associated with significantly increased urinary calcium, plasma parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D levels. Per 40 mg day(-1) of furosemide, urinary calcium was increased by 17% (P < 0.05) and plasma PTH levels were increased by 28% (P = 0.04). Users of LD had a 17% higher body weight (P < 0.001) compared with nonusers. This was due to a 32% higher fat mass (P < 0.001) and a 6% higher lean tissue mass (P < 0.001). Moreover, users of LD had a higher bone mineral density (BMD) at the spine (+7.5%, P < 0.001), hip (+4.8%, P = 0.004), forearm (+3.7%, P = 0.01) and whole body (+2.5%, P = 0.06). However, after adjustment for body weight differences, BMD did not differ between groups. Nevertheless, duration of LD treatment was positively associated with BMD at the spine (P = 0.03) and whole body (P < 0.05). BMD at the spine increases by 0.3% per 1 year of treatment. CONCLUSIONS: The increased renal calcium losses in users of LD are compensated for by a PTH-dependent increase in 1,25(OH)(2)D levels. Thereby calcium balance remains neutral without major effects on bone metabolism.

Aged↗
PubMed1986

Pharmacokinetics and diuretic effect of bumetanide following intravenous and intramuscular administration to horses.

Concentrations of the potent diuretic bumetanide were determined by a sensitive high performance liquid chromatographic procedure in plasma and urine from horses following intravenous and intramuscular administration of a dose rate of 15 micrograms/kg. The elimination half-life was found to be 6.3 min, the volume of distribution at steady state 68 ml/kg and the total plasma clearance 10.9 ml/min/kg. The onset of diuresis occurred within 15 min and diuresis was no longer apparent 1 h after i.v. administration. Given by the intramuscular (i.m.) route, bumetanide was rapidly absorbed; bioavailability was 70-80%. i.m. administration of bumetanide prolonged its plasma half-life (11-27 min) and enhanced and prolonged its diuretic effect.

Animals↗
PubMed1988

Effect of diuretics on ketamine and sulfanilate elimination in cats.

Rate constants of elimination were used to evaluate potential effects of diuretic agents on the elimination of ketamine from the blood of cats. Furosemide, mannitol, and aminophylline did not significantly alter the ketamine elimination rate constants, although the diuretics had a tendency to prolong elimination. This tendency of furosemide was further substantiated by observing the effect of furosemide on glomerular filtration. The rate of sulfanilate elimination, used as an indicator of glomerular filtration, was significantly decreased in the cats that were administered furosemide. Possible mechanisms for the influence of furosemide on the renal excretion of ketamine are discussed.

Aminophylline↗
PubMed1989

Diuretic effect induced by intrarenal infusion of nisoldipine in anaesthetized dogs.

1. Renal effects of nisoldipine, a potent calcium channel blocker, were examined in anaesthetized dogs. 2. Intrarenal arterial infusion of nisoldipine (10, 50 ng/kg per min) did not influence mean systemic blood pressure and renal haemodynamics, but did cause dose-related increases in urine flow and urinary excretion of electrolytes. During nisoldipine infusion at the higher dose, the levels of fractional excretion of sodium, potassium and chloride were significantly elevated. 3. In the lithium clearance study, fractional lithium excretion, an index of fractional sodium excretion in the proximal tubules, was unchanged even with the higher dose of nisoldipine, whereas fractional sodium excretion in the distal tubules markedly increased. 4. Nisoldipine elicited a significant increment in osmolar clearance without altering the reabsorption of free water. 5. Thus, intrarenal administration of nisoldipine at a non-hypotensive dose to anaesthetized dogs produced a significant diuretic effect without alteration in renal haemodynamics. Results in lithium clearance and free water clearance studies suggest that nisoldipine exerts a diuretic action by inhibiting sodium transport at the distal nephron segments beyond the proximal tubules.

Anesthesia↗
PubMed1990

Influence of diuretics on brachial artery diameter and distensibility in hypertensive patients.

Blood pressure, brachial artery diameter and pulse wave velocity were determined before and after diuretic treatment in 2 groups of hypertensive patients treated either by indapamide (2.5 mg per d) or by canreonate (50 mg per d). Brachial artery diameter, measured from pulsed Doppler flowmetry, and pulse wave velocity, evaluated from mechanography, did not alter significantly despite a significant blood pressure reduction. The study indicates that, in hypertensive patients of middle age, diuretics did not change brachial artery diameter and distensibility, whether the drug caused an increase or a decrease in plasma potassium levels.

Adult↗