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PubMed1983

Diuresis and pulmonary function in premature infants with respiratory distress syndrome.

A prospective study of 99 premature infants with severe respiratory distress syndrome who were randomly assigned to receive diuretic treatment with either furosemide or chlorothiazide was analyzed to examine the relationship of diuretic administration and diuresis to survival and to the duration and degree of mechanical ventilatory support. Subjects were given a diuretic, usually beginning on the second or third day of life, if they had not initiated the expected spontaneous diuresis and did not show pulmonary improvement. Infants given furosemide experienced a postnatal weight loss nearly identical to that in infants who were deemed not to need a diuretic; infants given chlorothiazide lost weight more slowly and had significantly greater body weight on postnatal days 4 and 5. Four factors were independently correlated with improved survival: furosemide usage, high birth weight, low initial mean airway pressure, and the absence of intraventricular hemorrhage. Ventilator mean airway pressure on the seventh day of life and duration of mechanical ventilation were both related to diuresis. These data provide additional evidence for the importance of water homeostasis in determining the course of respiratory distress syndrome in premature infants and indicate that furosemide administration is beneficial when spontaneous diuresis does not occur. Furosemide may be particularly effective if combined with early closure of the ductus arteriosus.

Chlorothiazide↗
PubMed1997

Infantile hypophosphatasia: treatment options to control hypercalcemia, hypercalciuria, and chronic bone demineralization.

A 2-month-old child with infantile hypophosphatasia had hypercalcemia (3.49 mmol/L (14 mg/dl)), nephrocalcinosis, and diminished bone mineral content. Hypercalcemia was corrected with calcitonin. Hypercalciuria and bone demineralization abated with chlorothiazide. Hypercalcemia is hypothesized to be related to normal bone resorption in conjunction with impaired bone mineralization. Chlorothiazide may alleviate this impairment.

Bone Resorption↗
PubMed1998

Spectrophotometric studies on the photostability of some thiazide diuretics in ethanolic solution.

First derivative and dual-wavelength spectrophotometric methods were used in the quantum yield determination of the photochemical decomposition reactions of three thiazide diuretics (chlorothiazide, hydrochlorothiazide and trichloromethiazide) in ethanolic solution. The radiation absorbed by the compounds was measured using iron(III) oxalate actinometry based on absorption spectrophotometry. An apparatus is described in which the drugs were irradiated in quartz cuvettes cooled by water in a stand built on a magnetic stirrer. The wavelength region available to the reaction cuvette was restricted to 313 nm with chemical potassium chromate filter solutions and a Corning filter plate. Chlorothiazide proved to be more photostable than hydrochlorothiazide and trichloromethiazide in ethanol.

Chlorothiazide↗
PubMed1987

Clopamide: plasma concentrations and diuretic effect in humans.

Clopamide pharmacokinetics were determined after oral doses of 5, 10, and 20 mg in normal volunteers. Maximum plasma concentrations occurred within 2 hours and were followed by a monoexponential decline with an elimination half-life of approximately 10 hours. There was an approximately linear relationship between dose and the AUC. Urinary sodium, chloride, and potassium excretion rates indicated that the peak diuretic activity corresponded with peak plasma drug concentrations and probably continued for 12 to 24 hours. There was little difference between the total sodium and chloride output after each dose of clopamide, suggesting that 5 mg may have been close to the top of the dose-response curve. Chlorothiazide, 500 mg, caused less sodium and chloride output with similar potassium loss. During chronic administration to patients with hypertension, hypokalemia was more marked with clopamide, 10 mg daily, than with clopamide, 5 mg, or chlorothiazide, 500 mg daily.

Administration, Oral↗
PubMed1979

Renal transport of oxalate: effects of diuretics, uric acid, and calcium.

Clearance experiments were performed in the rat to examine the effects of diuretics on the renal transport of oxalate. In addition, the effect of infusing either uric acid or calcium on the renal transport of oxalate was examined. During control periods, the fractional excretion of oxalate (FEOx) averaged 118.0 +/- 2.1%. Acute administration of either chlorothiazide, furosemide, or indanyl-oxyacetic acid (MK-196), a new uricosuric diuretic, resulted in a significant decrease in the FEOx in all groups to 104.8 +/- 2.4%, 111.3 +/- 2.1%, and 108.6 +/- 2.7%, respectively. Infusion of uric acid increased urinary uric acid excretion from 2.41 +/- 0.28 to 4.26 +/- 0.03 micrograms/min/g kidney wt (P less than 0.001) and decreased FEOx to 104.0 +/- 2.4% (P less than 0.001 compared to control). Infusion of calcium chloride increased urinary calcium excretion from 0.10 +/- 0.04 to 0.44 +/- 0.06 micrograms/min/g kidney wt (P less than 0.001) but had no effect on the FEOx which averaged 118.3 +/- 8.3% (P = NS compared to control). These studies show that the acute administration of chlorothiazide, furosemide, or MK-196, as well as increasing urinary uric acid excretion by uric acid infusion, are all associated with a decrease in the FEOx. Acutely increasing urinary calcium excretion, however, had no effect on oxalate transport.

Animals↗
PubMed1983

Renal calcium handling in familial hypocalciuric hypercalcemia.

We have determined calcium and sodium excretion rates in three members of a kinship with familial hypocalciuric hypercalcemia (FHH) and in four patients with primary hyperparathyroidism (PHP) under control conditions and following the intravenous administration of chlorothiazide or furosemide. The characteristic hypocalciuria of FHH, evidenced by a significantly reduced urinary calcium/creatinine ratio compared with that of PHP, is present under control conditions (0.08 vs. 0.26 mg calcium/mg creatinine, respectively, P less than 0.05), and after chlorothiazide (0.14 vs. 0.53, respectively, P less than 0.01). However, after furosemide infusion the calcium/creatinine ratio is no longer lower in FHH than in PHP (1.12 vs. 1.14, respectively, P greater than 0.05). These data suggest that, in FHH, tubular calcium reabsorption is enhanced in the thick ascending limb of Henle's loop, the site of action of furosemide. However, the data do not exclude the presence of an abnormality at a more distal site in the nephron.

Adult↗
PubMed1979

Diuretics, hepatic and thoracic duct lymph flows in the dog.

1. Simultaneous thoracic duct and hepatic lymph flows were measured in 29 mongrel dogs before and after the intravenous administration of mannitol, ethacrynic acid, frusemide and chlorothiazide in separate experiments. 2. Thoracic duct lymph flow increased significantly after each diuretic agent was administered. 3. Hepatic lymph flow increased only after ethacrynic acid and mannitol administration. Frusemide and chlorothiazide did not alter hepatic lymph flow. 4. These data show that increases in thoracic duct lymph flow after ethacrynic acid and mannitol arise partly from the liver, as well as from other organs.

Animals↗
PubMed1991

Effects of diuretics on stroke development in Kyoto-Wistar stroke-prone spontaneously hypertensive rats.

1. Previous studies have indicated that increases in dietary K+ promote diuresis and retard stroke development in stroke-prone spontaneously hypertensive rats (spSHR) fed a Japanese-style diet containing 4% NaCl. 2. It is possible that elevations in dietary K+ retard stroke development by inducing natriuresis and facilitating the clearance of Na+, and that diuretics associated with natriuresis might also be capable of retarding stroke development in spSHR. To test if this was the case, the onset of stroke development in spSHR fed a low (0.75%) K+ diet containing 4% NaCl (controls) was monitored and compared with that in spSHR treated with (a) frusemide, (b) chlorothiazide, (c) amiloride or (d) acetazolamide, and with (e) untreated spSHR fed a high (2.11%) K+ diet. 3. The onset of stroke, as well as death resulting from stroke, occurred at a significantly later age in spSHR fed a high K+ diet than in spSHR fed a low-K+ diet, despite the fact that both groups of spSHR rats had comparable blood pressures. 4. Treatment of spSHR with the above-named diuretics before stroke development did not alter the blood pressure of the rats. The onset of stroke development and death in spSHR treated with chlorothiazide, amiloride or acetazolamide was comparable with that observed in untreated control spSHR. In spSHR treated with frusemide, the onset of stroke was comparable with that of untreated control spSHR, whereas the onset of death after stroke development was accelerated. 5. Post mortems performed on spSHR that developed stroke indicated the presence of haemorrhagic stroke of comparable severity in the six groups of spSHR studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1988

The effect of diuretics on components of the urinary kallikrein-kininogen-kinin system in man.

The effects of acute infusions of diuretics on components of the human urinary kallikrein-kininogen-kinin system were determined. Normal human subjects were given infusions of chlorothiazide and furosemide in doses calculated to produce a comparable natriuresis and diuresis. Alterations in urine electrolyte excretion, kinins, total and intact kininogen, and total active kallikrein were determined before and after the diuretic administration. Chlorothiazide caused a significant increase in total, but not active, kallikrein and had no effect on kinins and total or intact kininogen. Furosemide did not alter total or active kallikrein, or intact kininogen, but did decrease kinin and total kininogen excretion significantly. These differences in effects were not related to urinary sodium excretion or urinary flow because both diuretics produced comparable effects on these parameters. We conclude that acute infusions of diuretics do not activate the kallikrein-kininogen-kinin system and that some of the previously described effects of diuretics on this system may be related to their site of action.

Adult↗
PubMed1989

Urinary angiotensin excretion during sodium restriction and diuretics.

The urinary excretion rate and plasma concentration of angiotensin I (UAI, PAI) and angiotensin II (UAII, PAII), and plasma renin activity (PRA) were measured in seven healthy volunteers in the supine and upright position both on free and restricted sodium intakes. The same variables were measured before and after intravenous injection of furosemide, as well as before and during intravenous infusion of chlorothiazide. Assumption of the upright posture as well as sodium restriction increased PAI, PAII, and PRA, but UAI and UAII excretion were not altered by these manoeuvres. Furosemide injection resulted in increases of all variables, albeit that PAI and PAII were elevated to a lesser extent then PRA. Chlorothiazide infusion caused a reduction in PAI, PAII, and PRA, whereas UAI and UAII excretion increased modestly. The discrepancies between changes in plasma and urinary AI and AII may indicate that urinary angiotensin excretion provides information which is supplementary to that of plasma angiotensins.

Adult↗
PubMed1981

Spironolactone therapy in infants with congestive heart failure secondary to congenital heart disease.

The efficacy of treatment with spironolactone for congestive heart failure secondary to congenital heart disease was studied in 21 infants under 1 year of age. All received digoxin and chlorothiazide. In addition, group A (n = 10) was given supplements of potassium and group B (n = 11) received spironolactone. Daily clinical observations of vital signs, weight, hepatomegaly, and vomiting were recorded. Paired t test analysis showed significant reduction in liver size and weight (P less than 0.01) and respiratory rate (P less than 0.05) in group B, and less significant decreases in group A. The incidence of vomiting was slightly lower in group B. We conclude that the addition of spironolactone hastens and enhances the response to standard treatment with digoxin and chlorothiazide in infants with congestive heart failure.

Chlorothiazide↗
PubMed1997

Expression of the sodium-chloride cotransporter in osteoblast-like cells: effect of thiazide diuretics.

The use of thiazide diuretics is associated with increased bone mineral density and, in some studies with reduced incidence of fractures, suggesting a potential role for these drugs in the treatment of osteoporosis. Our objective was to examine the effects of thiazides on osteoblast-like cells using the rat UMR-106 osteosarcoma cell line. Treatment of UMR-106 cells with chlorothiazide caused membrane depolarization and a rise of intracellular calcium but had no effect on adenosine 3,5'-cyclic monophosphate accumulation. The rise of intracellular calcium was partially inhibited by nifedipine and removal of extracellular calcium, indicating calcium uptake from the extracellular media, as well as by thapsigargin or dantrolene, indicating contributions from calcium release from intracellular stores. Reverse transcriptase-polymerase chain reaction was used to isolate a partial cDNA clone for the thiazide-sensitive sodium-chloride cotransporter from UMR-106 cells that hybridized to 5.0- and 11.0-kilobase mRNAs when Northern blot analysis was conducted. Antisense oligonucleotides to the sodium-chloride cotransporter specifically inhibited the chlorothiazide-induced depolarization and rise of intracellular calcium and reduced immunofluorescence staining for the sodium-chloride cotransporter protein in UMR-106 cells. We conclude that thiazide diuretics inhibit sodium-chloride cotransporter activity in UMR-106 cells, thereby altering intracellular calcium regulation. These results provide evidence for direct effects of thiazide diuretics on bone cells.

Animals↗
PubMed1985

Localization of diuretic action in microperfused rat distal tubules: Ca and Na transport.

Experiments were performed in rats to examine the distal site of action of thiazide diuretics and the additive hypocalciuric properties of thiazides and amiloride. In clearance experiments, the maximal natriuretic and hypocalciuric dose of chlorothiazide was established. When amiloride was added, there was further augmentation of Ca reabsorption (P less than 0.025) but no additional natriuresis. Amiloride blunted thiazide-induced kaliuresis (P less than 0.001). Localization of the thiazide effect was studied in early and late distal tubules microperfused in vivo with control and thiazide-containing solutions. The maximally effective luminal drug concentration, 5 X 10(-4) M, inhibited Na transport (P less than 0.001) and enhanced Ca transport (P less than 0.01) in the early distal segments; late segments were on the average unaffected. It is suggested that thiazides interact with the distal convoluted tubule cell, whose predominant location is the early distal tubule. In two long distal tubules, with early and late segments, a maximal concentration of chlorothiazide increased Ca transport and decreased Na transport. Addition of 10(-5) M amiloride caused an additional increment in Ca reabsorption. As amiloride's action is located in the late distal tubule, it is suggested from these experiments that a basis for additive hypocalciuric actions of thiazides and amiloride is separate sites of action in the distal tubule.

Absorption↗
PubMed1992

Luminal influences on potassium secretion: chloride, sodium, and thiazide diuretics.

In the presence of Cl-, K+ secretion by the distal tubule saturates with increasing luminal Na+ concentration. Apparent maximal K+ secretion is attained with luminal Na+ concentrations of 40 mM. The results of the present study show that lowering the Cl- concentration of luminal fluid can increase the level of Na(+)-stimulated K+ secretion beyond the maximal level attained in the presence of Cl-. The effect of lowering luminal Cl- concentration to less than 10 mM on K+ secretion is greater with higher Na+ concentration. Under these conditions, chlorothiazide decreases K+ secretion. When chlorothiazide is present, changing the Na+ concentration does not affect K+ secretion. Because in rats a thiazide effect is attributed primarily to the distal convoluted tubule (DCT), we postulate that it is primarily DCT cells that increase K+ secretion when Na+ concentration is raised in the presence of low luminal Cl- concentration. We propose that the rat DCT cells have both an absorptive Na(+)-Cl- cotransport mechanism and a secretory K(+)-Cl- cotransport mechanism in the luminal membrane that can mediate the apparent exchange of Na+ for K+.

Animals↗
PubMed1986

Pharmacologic probing of renal development in the neonatal rat.

This study was designed to examine the ontogeny of renal functions in the neonatal rat using various pharmacologic agents as probes. The renal responses of 2-, 6-, and 10-day-old rats to diuretic agents known to act on proximal tubules, loops of Henle and distal tubules were assessed. These included acetazolamide, furosemide, mercaptomerin, chlorothiazide and amiloride. Following administration of a diuretic agent, urine was collected at 90-min intervals for 6 h and urine volume, osmolality, chloride and pH were measured. Acetazolamide, furosemide, chlorothiazide and amiloride induced diuresis at each age indicating that the respective reabsorptive mechanisms were present and functional by 2 days of age. At all ages furosemide evoked a maximal response in eliminating the interstitial fluid gradient as indicated by the formation of an isosmotic urine in treated pups. However, the volume of the diuresis at 2 days of age was half those at 6 and 10 days, reflecting enhanced activity of the countercurrent multiplication apparatus in the maturing pups. Administration of mercaptomerin did not produce pharmacologic diuresis, but rather resulted in acute renal failure; although the nephrotoxicity was to a lesser extent in 2-day-old pups. The ability of the neonatal rat to respond to these pharmacologic probes demonstrates that the integrity of these renal functions is established in this species early in postnatal life.

Acetazolamide↗
PubMed1983

Natriuretic activity of human and monkey atria.

Recent evidence indicates that mammalian atria contain a substance that produces a rapid onset natriuresis in anesthetized rats. In the present experiments, small portions of human right atria obtained from patients undergoing coronary bypass surgery, as well as monkey atria and ventricles obtained from the Regional Primate Center, Seattle, were boiled or acid extracted and lyophilized. These materials (30 mg/kg) were dissolved in Ringer's lactate and injected intravenously into anesthetized monkeys to determine their effects on renal function. Their effects were also compared with those of furosemide (0.1 mg/kg) and chlorothiazide (10 mg/kg). Human and monkey atrial extracts produced significant increases in sodium and calcium excretion that were independent of changes in creatinine clearance. Monkey ventricular extract had no consistent renal effects. Furosemide, but not chlorothiazide, mimicked the renal responses to human and monkey atrial extracts in terms of time of onset, duration, and pattern of electrolyte excretion. These data suggest that primate atrial tissue contains a heat- and acid-stable natriuretic factor similar to that first described in the rat, suggesting that mammalian atrial natriuretic factors are cross-reactive among species. In addition, atrial natriuretic factors may have a mechanism of action similar to that of furosemide.

Animals↗
PubMed1973

Pyrazinoate excretion in the chimpanzee. Relation to urate disposition and the actions of uricosuric drugs.

These experiments were designed to define the renal disposition of pyrazinoic acid in a nonhuman primate that is phylogenetically close to man and to relate this to the effects of pyrazinoate on urate excretion. The renal clearance of pyrazinoate was almost always greater than the simultaneous glomerular filtration rate at plasma concentrations ranging from 1.9 to 960 mug/ml. Some inhibitors of tubular secretion, probenecid, MK-282 (an experimental, potent uricosuric drug), p-aminohippurate, iodopyracet, sulfinpyrazone, and mersalyl, reduced clearances of pyrazinoate to values far below filtration rate. Chlorothiazide, allopurinol, and salicylate did not. The clearance of pyrazinoate was not influenced by changes in urine flow. It is concluded that pyrazinoate is actively secreted and actively reabsorbed. Pyrazinoate had a dual effect on urate excretion. At concentrations in plasma less than 10 mug/ml there was a concentration related fall in urate/inulin clearance ratio, reaching values of 10-20% of control. Over the range of 10-100 mug/ml in plasma, the clearance of urate remained maximally depressed. At higher concentrations of pyrazinoate there was a concentration related increase in urate/inulin clearance ratio such that at pyrazinoate levels above 600 mug/ml a definite uricosuric response was obtained. Prior administration of pyrazinoate to give plasma levels of 20-140 mug/ml completely or almost completely prevented uricosuric responses to probenecid, PAH, chlorothiazide, and sulfinpyrazone. Iodopyracet, mersalyl, salicylate and N-acetyl-4-dibutylsulfamoyl-3-trifluoromethylbenzenesulfonamide (MK-282) retained significant uricosuric action, but the activities were probably less than normal. The results are consistent with a model of urate transport involving high rates of bidirectional transtubular flux.

Allopurinol↗
PubMed1978

Further studies on segmental sodium transport in the rat kidney during expansion of the extracellular fluid volume.

The present studies were designed to further investigate the possibility of heterogeneity of nephron function during Ringer loading in the rat, and to determine the specific nephron segment responsible for this finding. As in previous studies from this laboratory with smaller rats (50-125 g), net addition of sodium between late distal tubule and papillary base (6.9 vs. 10.4% of the filtered load, respectively, P <0.005) was found in more mature rats (170-230 g). In contrast, there was net reabsorption of sodium between these two segments in nonvolume-expanded animals, 1.70 vs. 0.45% of the filtered sodium load, P <0.005. Because nephron heterogeneity of sodium transport during extracellular volume expansion is the most likely explanation for these findings, further studies were performed to determine the specific juxtamedullary nephron segment responsible for the net addition pattern between late distal tubule and papillary base in Ringer-loaded animals. First, a comparison was made of sodium delivery to the late proximal tubule of superficial nephrons vs. the delivery rate to the bend of Henle's loop of juxtamedullary nephrons in both hydropenia and Ringer loading. Fractional sodium delivery was quite comparable between the superficial and juxtamedullary nephrons in both hydropenia and Ringer loading although the absolute level was much greater in both groups of nephrons in the Ringer studies. Chlorothiazide (15 mg/kg loading and 15 mg/kg per h) given during Ringer loading markedly increased late distal sodium delivery, 19% of the filtered load, but did not prevent net addition of sodium at the papillary base. In contrast, furosemide (5 mg/kg loading and 5/mg/kg per h) given during Ringer loading completely reversed the segmental pattern, 35.5 and 28.8% at late distal tubule and papillary base, respectively, P <0.005. These studies demonstrate that the net addition of sodium between late distal tubule and papillary base during Ringer loading is not limited to immature rats and that the segmental pattern does not occur in non-volume-expanded animals. Further, the reversal of the net addition pattern with furosemide, but not chlorothiazide, and the comparable proximal nephron delivery rates in Ringer loading suggest that the loop of Henle of juxtamedullary nephrons reabsorbs less sodium than the same portion of superficial nephrons in this setting. A model is proposed to explain this finding.

Animals↗