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PubMed1962

On the metabolism of methylated disulphonamides with a diuretic action. A contribution to the mechanism of action of chlorothiazide and similar compounds.

The metabolism of two substances possessing a diuretic action, 4-amino-6-chlorobenzene-1,3-disulphonmethylamide (III) and 6-chloro-3,4-dihydro-2-methyl-7-methylsulphamoyl-2H-1,2,4-benzo[e]thiadiazine-1,1-dioxide (IV), has been studied on rats and human subjects. It has been shown that these compounds are not demethylated in the -SO(2).NHCH(3) group. They therefore do not act through liberation of substances with unsubstituted sulphonamido-groups which might inhibit carbonic anhydrase, and their mechanism of diuretic action cannot be considered due to inhibition of this enzyme.

Animals↗
PubMed1971

Responses of mean arterial pressure to pressor agents and diuretics in renal hypertensive and salt hypertensive rats.

1. The responses of the mean arterial pressure to (-)-noradrenaline, tyramine, angiotensin II-val(5)-amide, vasopressin and rat renin have been contrasted in renal hypertensive and in salt plus desoxycorticosterone hypertensive rats. The responses were measured in rats both unanaesthetized and rats anaesthetized with pentobarbitone.2. Responses of unanaesthetized, ganglion blocked renal hypertensive rats to noradrenaline, tyramine and vasopressin markedly exceeded, and to angiotensin II and renin were markedly smaller than, those of unanaesthetized ganglion blocked salt + DOC hypertensive animals. Responses to angiotensin and to renin were apparently enhanced in the latter animals.3. Hydrochlorothiazide and frusemide markedly reduced mean arterial pressure in salt + DOC hypertensive rats before and after ganglionic blockade.4. Neither diuretic caused significant reduction in the mean arterial pressures of unanaesthetized, renal hypertensive rats in the absence of ganglionic blockade: frusemide did so in anaesthetized and unanaesthetized rats after ganglionic blockade.5. Whereas the diuretics did not affect the responses of the renal hypertensive rats to pressor agents, frusemide and to a lesser extent hydrochlorothiazide tended to depress the responses to pressor agents in salt induced hypertension.6. Hydrochlorothiazide did not influence mean arterial pressure in unanaesthetized rats with neurogenic hypertension.

Anesthesia, General↗
PubMed1972

Renal excretion of metolazone, a new diuretic.

1. Metolazone, a new diuretic, was found to be excreted by glomerular filtration and renal tubular secretion.2. The secretory mechanism was antagonized by probenecid but this did not affect the diuretic action of metolazone.

Animals↗
PubMed1981

BTS 39542, a dihydrophthalazin-1-ylacetic acid with high efficacy diuretic activity.

1 BTS 39542, a novel dihydrophthalazin-1-ylacetic acid, has high efficacy diuretic activity in mice, rats, rabbits and dogs. It is twice as potent as frusemide in mice and dogs, ten times as potent in rats and twenty times as potent in rabbits. 2 BTS 39542, like frusemide, exerts its major effects in the loop of Henle and increases renal blood flow but does not affect glomerular filtration rate in dogs. 3 The ratio of the excretion of the major cations (sodium plus potassium) to that of the major anion (chloride) after either BTS 39542 or frusemide varied with species. In rats and rabbits the ratio was approximately unity but in mice and dogs the ratio consistently exceeded unity. 4 A method for evaluating diuretics based on potency and relative potassium excretion is described.

Animals↗
PubMed1993

The diuretic action of 8-cyclopentyl-1,3-dipropylxanthine, a selective A1 adenosine receptor antagonist.

1. The diuretic effect of the selective A1 adenosine receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (CPX), was investigated in anaesthetized rats. 2. CPX (0.1 mg kg-1, i.v.) produced significant increases in urine flow, and the excretion rate and fractional excretion of both sodium and chloride. By contrast, CPX administration did not result in any significant change in the excretion of potassium. 3. The diuretic effect of CPX was accompanied by a transient increase in inulin clearance although p-amino-hippurate clearance was unaffected, indicating the CPX induced a temporary elevation of glomerular filtration rate but no change in renal blood flow. 4. The fractional excretion of lithium (a marker of delivery of fluid out of the proximal tubule) was also significantly increased by CPX. However, other measures of tubular function derived from lithium clearance indicated that there were no changes in the handling of sodium or water in the distal regions of the nephron. 5. CPX did not significantly alter the relationship between either free water reabsorption or free water clearance and the distal delivery of sodium, which suggests that CPX does not affect the renal concentration/dilution mechanism. 6. The results of this study show that the diuresis and increased excretion of sodium and chloride induced by CPX (0.1 mg kg-1) in the rat, occurs with only transient elevation in glomerular filtration rate and no change in renal blood flow. The primary reason for the diuresis appears to be inhibition of sodium reabsorption in the proximal tubule. Furthermore, the results provide evidence that production and release of endogenous adenosine modifies renal excretory function via stimulation of the A1 receptor subtype.

Animals↗
PubMed2005

Role of HSD11B2 polymorphisms in essential hypertension and the diuretic response to thiazides.

BACKGROUND: The renal 11beta-hydroxysteroid dehydrogenase type 2 (11beta HSD2) enzyme inactivates 11-hydroxy steroids in the kidney, thereby protecting the nonselective mineralocorticoid (MR) receptor from occupation by glucocorticoids. Loss-of-function mutations in the gene encoding 11beta HSD2 (HSD11B2) result in overstimulation of the MR and cause salt-sensitive hypertension. METHODS: We have investigated the role of HSD11B2 in hypertension in 377 genetically homogeneous essential hypertensives from North Sardinia. RESULTS: Thirty of these patients displayed increased urinary cortisol metabolite ratios (greater than or equal to 2) (tetrahydrocortisol [THF]+allotetrahydrocortisol [aTHF]/tetrahydrocortisone [THE]) reflecting a mild reduction in 11beta HSD2 activity. No mutations in HSD11B2 were detected in these patients. All 377 patients were genotyped for a CA repeat microsatellite in intron 1 of HSD11B2 and a G534A polymorphism in exon 3 of HSD11B2. CA repeat length was associated with the (THF+aTHF)/THE ratio, which in turn was significantly related to PRA levels. No associations were found between the G354A polymorphism and the other parameters. There were no differences in blood pressure (BP) levels between HSD11B2 genotypes, but in a subgroup of 91 patients that underwent diuretic therapy, CA repeat length was strongly associated with the BP response to hydrochlorothiazide. CONCLUSION: This study highlights the role of this HSD11B2 polymorphism in sodium handling and is consistent with a role in the BP response to thiazide diuretics.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗
PubMed1976

Change in antikaliuretic response to potassium-sparing diuretics in patients with cirrhotic ascites.

In 2 elderly patients with ascites due to hepatic cirrhosis, potassium excretion decreased during re-administration of potassium-sparing diuretics after recurrence of ascites following withdrawal of previous prolonged treatment. An exaggerated antikaliuretic response and a paradoxic rise in potassium excretion are "unpredictable" changes which may occur during administration of potassium-sparing diuretics at different times in the same patient treated with the same drug.

Aged↗
PubMed1991

Effects of tobacco and diuretics on human palatal salivary glands.

The prevalence of macrophotographically documented sialadenitis in the palatal mucosa of 184 probands, aged 23 yr or older, was studied in the Koster Health project. A total of 75 (mean age 58.9) revealed inflammatory changes around the duct orifices of the palatal glands. In 10, biopsies were performed for histomorphologic analyses to confirm the diagnosis of sialadenitis. Statistics with matched pairs showed a significantly higher ratio of tobacco use among individuals with sialadenitis than among those with clinically unchanged palatal gland orifices. A relationship between the use of diuretics and sialadenitis was also statistically significant. It can be concluded that tobacco use and diuretics may induce inflammatory changes in the palatal glands and that macrophotography of the palatal mucosa may serve as a valuable, non-invasive method for scoring sialadenitis.

Adult↗
PubMed1984

Aspects on pharmacokinetics of some diuretics.

This review summarizes the present knowledge of some commonly used diuretics. Bendroflumethiazide and bumetanide are completely absorbed from the gut while the uptake of hydrochlorothiazide, chlorthalidone and furosemide averages about 65%. The degree of uptake of amiloride and spironolactone is unknown but exceeds 50%. Plasma t 1/2 of bumetanide and furosemide are approximately 1 h. The clinically important phase of the plasma concentration of bendroflumethiazide has a t 1/2 of 3 h, although a slower phase with a t 1/2 of 9 h has been described. Hydrochlorothiazide and amiloride, often used in combination, both have a t 1/2 of about 10 h. Canrenone, an active metabolite of spironolactone, has a t 1/2 of 15-20 h. Chlorthalidone is eliminated very slowly with a t 1/2 of about two days. This is partly caused by an extensive binding to carbonic anhydrase in the erythrocytes. The protein binding of bendroflumethiazide, bumetanide, canrenone and furosemide is approximately 95%. The binding of chlorthalidone and hydrochlorothiazide is about 75 and 40% respectively. All mentioned diuretics except spironolactone are in part eliminated renally, mainly via tubular secretion. This is the major elimination route for amiloride and hydrochlorothiazide, while it constitutes one third to two thirds for bendroflumethiazide, bumetanide and furosemide. Spironolactone is exclusively eliminated as metabolites.

Amiloride↗
PubMed1984

Hemodynamic effects of diuretic therapy in hypertension.

The antihypertensive effect of diuretics is well documented. At least some preserved kidney function seems to be necessary to achieve a demonstrable effect. The importance of fluid volume reduction for the antihypertensive effect of these drugs during long-term treatment is however uncertain. The effects on central hemodynamics vary according to the literature, but the blood pressure reduction in responders (delta MAP greater than 10%) may primarily be explained by a reduction of the total peripheral vascular resistance. The peripheral circulation is influenced in the same way. Sometimes a flow reduction is observed, and sometimes a resistance reduction. In spite of a lasting blood pressure reduction after treatment with diuretics, the structural hypertensive vascular changes do not seem to be influenced.

Body Fluids↗
PubMed1984

Intraerythrocyte sodium content and transmembrane sodium flux in hypertensive patients treated with diuretics or beta-adrenoceptorblockers.

Forty-seven male patients with essential hypertension were randomized to treatment with either a beta-adrenoceptorblocker (metoprolol), (n = 24), or a diuretic (hydrochlorothiazide), (n = 23). If their diastolic blood pressure was not lowered below 95 mm Hg by the maximum dose of either drug, hydralazine (15 patients) and in a few cases (6 patients) spironolactone was given. After five years of treatment all the patients were examined with respect to intraerythrocyte sodium (IeNa) and potassium (IeK), sodium influx and sodium efflux. Patients treated with the diuretic (D) tended to have a higher IeNa (9.8 +/- 0.4 mmol/l red cells) and sodium influx (0.044 +/- 0.002 mmol Na/l X min) compared with those taking the beta-adrenoceptorblocker (B) (8.9 +/- 0.3 mmol/l and 0.041 +/- 0.002 mmol Na/l X min), but neither of these differences was statistically significant. Sodium efflux, however, was significantly increased in D (0.073 +/- 0.003 mmol Na/l X min vs 0.061 +/- 0.003 mmol/l X min). No difference in IeK was noted between the two groups. Six patients taking spironolactone had a low IeNa (7.3 +/- 0.4 mmol/l), sodium influx (0.039 +/- 0.001 mmol Na/l X min) and sodium efflux (0.050 +/- 0.006 mmol Na/l X min).

Adrenergic beta-Antagonists↗
PubMed1984

Problems with potassium and magnesium in diuretic-treated patients.

Treatment with thiazides and loop diuretics increase the urinary excretion of potassium and magnesium and the body content of these ions are reduced after long-term treatment. The diuretic-induced magnesium deficiency influences the potassium metabolism. Magnesium is a necessary activator of Na-K-ATPase, which supplies the Na-K pump with energy. Lack of magnesium will therefore impair the pumping of sodium out of the cell and of potassium into the cell. The change of the relationship between extra and intracellular potassium may induce cardiac arrhythmias. Certain groups of patients, such as patients on digitalis therapy, patients with secondary hyperaldosteronism, elderly patients with insufficient dietary habits, and heavy drinkers, run an additional risk of developing potassium/magnesium disturbances. In young patients with uncomplicated essential hypertension, the risk is probably very small.

Diuretics↗
PubMed1989

Chemical structure and toxicity of diuretics in isolated hepatocytes.

The effects of several diuretics, including tienilic acid and indacrinone, on isolated rat heaptocytes were examined. Addition of tienilic acid and indacrinone at 1 mM to a suspension of freshly isolated cells caused dose-dependent loss of cell viability as judged by the LDH-latency test. Survey of 19 structurally related compounds revealed that the extent of cell injury and chemical structure were correlated, and an intense adverse effect was attributed to the 2-thienylcarbonyl moiety. Several other factors influencing cell viability are also disclosed. Further study revealed that tienilic acid and indacrinone were toxic to the primary culture of hepatocytes at a lower dose than that a freshly isolated hepatocytes. Thus, an isolated hepatocyte system can be used to select compounds displaying low hepatotoxicity, as for example is needed when screening diuretics.

Animals↗
PubMedDate not supplied

Phototoxicity to sulphonamide-derived oral antidiabetics and diuretics: investigations in hairless mice.

The oral antidiabetics glibenclamide, glipizide, glymidine, tolazamide and tolbutamide and the diuretics bemetizide, bendroflumethiazide, benzylhydrochlorothiazide, bumetanide, butizide, furosemide, hydrochlorothiazide, hydroflumethiazide and trichlormethiazide were investigated for phototoxic effects in hairless mice. The back of the animals (hr/hr-c3H/TifBom) was covered with Duoderm dressing, and at the site of two punched out holes 0.05 ml of the test substances at 0.25 mol/l concentration and the solvent alone as control were injected intradermally, respectively. Both test and control sites were irradiated with 6-12 J/cm2 of longwave UVA light from a "Bluelight 2000" apparatus (Hönle, Martinsried, Germany). Skin reactions were read at 24 and 48 h. Compared to the solvent alone, all of the test substances induced reactions (necrosis or oedema)--most frequently seen by macroscopic and histologic investigation and by measurements with a thickness gage. Injection of the test substance or solvent alone without or with subsequent UVA irradiation, as well as UVA alone, did not induce measurable skin changes in this model. Three oral antidiabetics and four diuretics, not yet described to induce photosensitivity in vitro nor in vivo, were detected as potential photosensitizers using our animal model.

Animals↗
PubMed2006

Diuretic-induced hypokalaemia in patients with hypertension.

We describe a 55 year-old woman with longstanding hypertension who developed hypokalaemia following diuretic treatment. Investigations revealed primary hyperaldosteronism due to an adrenal adenoma, and normal blood pressure was restored after surgical removal of the tumour. Primary hyperaldosteronism is a potentially curable cause of hypertension and should be considered in hypertensive patients who present with diuretic - induced hypokalaemia.

Adrenal Cortex Neoplasms↗
PubMed1984

Effects of standard diuretics and ortho-vanadate on sodium transport across isolated frog skin.

Frog (Rana temporaria) skins were studied in an Ussing type lucite chamber adapted to diminish tissue edge damage. The transepithelial electrical potential difference, short circuit current and direct current (DC) resistance of skins mounted in this chamber were 56, 20 and 24% higher, respectively, than those of skins mounted in a conventional chamber. Amiloride, triamterene, ouabain and ortho-vanadate inhibited short circuit current and net mucosal to serosal flux of 22Na. Amiloride and triamterene had rapid onsets of action and were effective only when administered to the mucosal (pond) side of the skin. Ouabain and ortho-vanadate had slower onsets of action and were effective only when administered to the serosal side of the skin. Steady state of effects of these drugs was not reached within the three-hour period of the experiments. The inhibitory effect of ortho-vanadate was blocked by adding a disulfonic stilbene derivative (DIDS) to the serosal side of the skin. Serosal prostaglandin E2 stimulated the short-circuit current and decreased the DC resistance. Thiazides, acetazolamide and loop diuretics had no effects on Na+ transport by frog skin. Thus, frog skin seems to be a useful model only in studies of the mode of action and the structure-activity relationship of diuretic which act by inhibiting sodium entry or Na+-K+-ATPase activity.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1990

The effect of loop diuretics on the long-term outcome of post-ischaemic acute renal failure in the rat.

The effects of continuous treatment with loop-acting diuretics on the long-term functional and histopathological outcome in kidneys subjected to 45 min of warm ischaemia were studied. One month after the primary damage the inulin clearance in the untreated kidneys was 0.44 +/- 0.05 ml min-1, improving significantly to 0.69 +/- 0.11 ml min-1 in furosemide-treated animals and to 0.75 +/- 0.09 ml min-1 in those treated with piretanide. Urine osmolality increased from 986 +/- 89 mosmol kg-1 in the untreated animals to 1479 +/- 195 mosmol kg-1 in the furosemide-treated ones. At the same time the total area of the outer medulla occupied by Tamm-Horsfall protein cylinders decreased from 7.0 +/- 1.2% in the untreated animals to 3.6 +/- 0.52% in the treated ones. It is concluded that by decreasing the number of nephrons blocked by Tamm-Horsfall cylinders an improvement in the function of ischaemically damaged kidneys can be achieved. This blockade, also called secondary damage, is of critical prognostic importance for the long-term outcome of the ischaemic renal failure. Treatment of the animals with loop diuretics decreased the occurrence of these cylinders, leading to an improvement of kidney function I month after the primary damage, this despite the fact that the primary damage seen in the early recirculation period was not treated specifically.

Acute Kidney Injury↗
PubMed2002

A case report of acute heart failure caused by a patient delaying taking his diuretic medication.

Acute heart failure is a life-threatening medical emergency, most commonly occurring as an immediate or delayed complication of acute myocardial infarction (AMI), or resulting from severe hypertension or valvular defects (stenosis or incompetence). Occasionally it is caused by patients' non-compliance with medication orders. In this case the patient had a history of three previous AMIs, controlled hypertension, and controlled congestive heart failure (CHF) for which he took two 40 mg frusemide tablets (a very potent oral diuretic) each morning. Because he had experienced bladder discomfort during the latter stages of previous appointments he decided to delay taking the diuretic until after his appointment and acute heart failure ensued.

Acute Disease↗