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PubMed1993

Effect of various diuretics on membrane voltage of macula densa cells. Whole-cell patch-clamp experiments.

The tubuloglomerular feedback mechanism is inhibited by diuretics such as furosemide. For the macula densa (MD) cells similar transport systems, as present in thick ascending limb (TAL) cells, have been suggested. To examine this further, membrane voltages (Vm) of MD cells were recorded with the fast or slow whole-cell patch-clamp method. The effects of diuretics on voltages and the conductance properties of these cells were examined. Vm of MD cells measured with the whole-cell patch-clamp method were as high as those in TAL cells: -72 +/- 1 mV (n = 21). An increase in the extracellular K+ concentration by 15 mmol/l depolarized Vm of MD cells by 11 +/- 1 mV (n = 18). Ba2+ (1 mmol/l) reversibly depolarized MD cells by 10 +/- 2 mV (n = 10). Thus, MD cells possess a K+ conductance that could allow for the recycling of K+ taken up by the Na(+)-2 Cl(-)-K+ cotransporter. MD cells hyperpolarized reversibly upon addition of the loop diuretics furosemide, piretanide and torasemide, whereas muzolimine and hydrochlorothiazide, neither one acting on this cotransport system in other preparations including the TAL, had no effect on Vm. MD cells most likely possess the same cotransport system as the TAL cells, which drives NaCl reabsorption in the TAL and serves as sensor for the tubular NaCl concentration in MD cells.

Animals↗
PubMed1986

The significance of the relative effects of loop diuretics and anti-brain edema agents on the Na+,K+,Cl- cotransport system and the Cl-/NaCO3- anion exchanger.

3-Amino-5-sulfamoylbenzoic acids and several series of (aryloxy)alkanoic acids were evaluated for their inhibitory effects on two human erythrocyte ion transport systems--the Na+,K+ cotransport system and the DIDS-sensitive anion carrier. Several classic loop diuretics, including the (aryloxy)alkanoic acid-ethacrynic acid and several 3-amino-5-sulfamoylbenzoic acids, like bumetanide and furosemide, displayed relatively strong inhibitory activity versus the cotransport system with relatively weaker action versus the anion carrier. Furthermore, diuretic potency correlated with cotransport inhibitory potency. Another class of (aryloxy)alkanoic acids, namely the [(2,3-dihydro-1H-inden-5-yl)oxy]acetic acids, such as indacrinone and MK-473, which exhibit less potent loop diuretic activity, were less potent cotransport inhibitors and more effective inhibitors of the anion carrier. Still other (aryloxy)alkanoic acids, with little saliuretic activity, namely a sub-class of [(2,3-dihydro-1H-inden-5-yl)oxy]alkanoic acids and a series of [(2,3,9,9a-tetrahydro-1H-fluoren-7-yl)oxy]acetic acids displayed little or no inhibitory action on the cotransport system but enhanced inhibitory action on the anion carrier. Most interestingly, the relative anion carrier inhibitory potency correlated well with the relative inhibitory activity of each compound on bicarbonate-stimulated cell swelling in cat cerebrocortical slices.

Bumetanide↗
PubMed1978

Effects of ozolinone, a diuretic active metabolite of etozoline, on renal function. I. Clearance studies in dogs.

The renal action of 3-methyl-4-oxo-5-piperidino-thiazolidine-2-ylidine (ozolinone), a metabolite of the diuretic etozoline (Elkapin), was studied in anaesthetized dogs after i.v. injection and compared with the renal effects of furosemide. The diuretic action of ozolinone was rapid in onset and of short duration. The smallest effective i.v. dose was 1 mg . kg-1. Maximal diuretic capacity was reached at 50 mg . kg-1 i.v. Fractional tubular sodium reabsorption was depressed to 67% at maximal effective doses. Ozolinone had similar renal actions to those of furosemide. Like furosemide, ozolinone increased renal blood flow, slightly decreased glomerular filtration rate, depressed tubular chloride reabsorption more than sodium reabsorption, increased potassium excretion, lowered the pH of urine, decreased urinary osmolarity towards isotonicity and depressed tubular PAH secretion. As regards the effective doses and the maximal changes of tubular sodium excretion, ozolinone was somewhat less potent than furosemide.

Animals↗
PubMed1986

Study of the tolerance and diuretic properties of torasemide following oral or intravenous administration to healthy volunteers.

The tolerance and diuretic properties of torasemide after oral or intravenous administration to healthy volunteers were studied. Six groups, each of 6 subjects, were given single rising oral doses ranging from 10 to 100 mg; 8 subjects received ascending i.v. doses on alternate days, ranging from 2.5 to 80 mg. At the highest oral doses investigated (80 mg and 100 mg) a number of volunteers complained of cramps in the knees, calves and feet. These symptoms were generally of short duration. Similar effects were not encountered during the intravenous study. There were no significant changes in ECG. Some significant drug-related changes were encountered in the within-study biochemistry and haematology assessments. Torasemide proved to be a potent diuretic following oral administration at all the doses investigated and following intravenous administration at all doses except 2.5 mg. A linear relationship existed between the urine output and the logarithm of the dose, and both sodium and chloride excretion were linearly correlated with urine volume. The rate of potassium excretion was markedly lower than that of sodium and chloride and was linearly correlated with the logarithm of the urine volume. Torasemide was well tolerated from all perspectives studied. It showed a potent diuretic property, and was equally effective by the oral and intravenous routes.

Administration, Oral↗
PubMed1988

The effect of diuretic therapy on adrenaline-induced hypokalaemia and hypomagnesaemia.

We have examined the interaction between the administration of bendrofluazide, frusemide, spironolactone, and placebo and increased plasma adrenaline concentrations in a double-blind, placebo-controlled, cross over study. We studied healthy subjects on the fourteenth day of each treatment period and after a two hour infusion of adrenaline (0.06 micrograms.kg-1.min-1 [0.33 nmol.kg-1.min-1]) we measured their heart rates, blood pressures, and plasma potassium and magnesium concentrations. There were no differences in heart rates or blood pressures for all four treatments. Baseline potassium concentrations were not significantly different compared to placebo, and plasma potassium fell during the period of the infusion on all study days. this fall was significantly greater on frusemide (0.5 mmol.l-1) and bendrofluazide (0.4 mmol.l-1) compared with both placebo and spironolactone. Baseline plasma magnesium concentration were not different and similar falls in plasma magnesium were seen on all four treatments during and after the adrenaline infusion. We conclude that chronic diuretic therapy with a thiazide diuretic or frusemide may increase the severity of hypokalaemia during short-term rises in plasma adrenaline. Pretreatment with spironolactone had no effect on adrenaline-induced hypokalaemia. None of the diuretics studied altered adrenaline-induced hypomagnesaemia.

Adult↗
PubMed1980

Studies with the optically active isomers of the new diuretic drug ozolinone. II. Inhibition by d-ozolinone of furosemide-induced diuresis.

The effect of the non-diuretic dextrorotatory isomer of ozolinone on furosemide-induced diuresis was studied by means of clearance and micropuncture techniques in rats. After intravenous injection, d-ozolinone antagonized the furosemide-induced increase in renal fluid and electrolyte excretion in a dose-related manner. Microperfusion experiments of Henle's loop in vivo revealed that d-ozolinone did not interfere with the action of furosemide at this tubular site. However, d-ozolinone markedly decreased the furosemide to inulin clearance ratio, presumably as a consequence of inhibition of furosemide secretion into the proximal tubules. It is assumed that, in consequence of a high affinity for the proximal organic acid transport system, d-ozolinone depresses proximal tubular furosemide secretion and prevents transfer of this diuretic to the tubular fluid. Thus, under the influence of d-ozolinone, furosemide cannot reach the loop of Henle in sufficient amounts and its diuretic effect is blocked.

Animals↗
PubMed1981

Human plasma vasopressin response to potent loop-diuretic drugs.

To investigate the effect of potent loop diuretic drugs on the factors that control water excretion, immunoreactive plasma arginine vasopressin was measured at regular intervals for 6 h after intravenous administration of frusemide (40 mg) and piretanide (12 mg) in healthy adults. Despite a large diuresis there was no significant rise in plasma vasopressin compared to controls. Diuretic drug treatment caused small increases in plasma osmolality comparable to the control group, but no change in mean arterial blood pressure. The fall in blood volume of 7% within 1 h of frusemide administration was insufficient to stimulate vasopressin secretion. We conclude that loop diuretic drugs in the dose given have little effect on plasma vasopressin and osmolality but cause a small fall in blood volume in healthy adults.

Adult↗
PubMed1988

Ketanserin combined with a beta-blocker or diuretic in essential hypertension. A multicentre study.

The antihypertensive effect of ketanserin 40 mg b.d. in combination with a beta-adrenergic blocking agent or a diuretic was assessed in an open study in 35 patients with essential hypertension, who had not responded to treatment with beta-blockers, diuretics or their combination. The ketanserin/beta-blocker combination decreased mean sitting systolic/diastolic blood pressure (SBP/DBP) from 169/107 mmHg to 156/91 mmHg at the end of the 12-week active treatment period. The decrease in systolic blood pressure was significant only at Week 8, while the decrease in diastolic blood pressure was highly significant at all times. A significant reduction in heart rate by 10 beats.min-1 was observed with the ketanserin + beta-blocker combination. The ketanserin/diuretic combination led to a significant reduction in mean SBP/DBP from 164/106 mmHg to 146/92 mmHg after 12 weeks, with no significant change in heart rate. Body weight slightly increased in both groups. There were significantly fewer adverse reactions with the ketanserin/diuretic combination than with the ketanserin/beta-blocker combination. The results indicate a potentially useful therapeutic role for ketanserin in combination with beta-blockers or diuretics.

Adrenergic beta-Antagonists↗
PubMed1993

Central hemodynamic effects of diuretic therapy in chronic heart failure.

In chronic heart failure diuretic drugs improve central hemodynamic variables and cardiac pumping secondary to altered plasma and extracellular volumes; humoral markers of these changes include increased plasma renin and aldosterone levels. The latter increases are maximal over the first week but decline with chronic therapy. The plasma alpha-ANP levels show a reciprocal effect; these data are compatible with a rapid contraction of the plasma volume which is sustained during chronic therapy. The acute hemodynamic actions of diuretic agents reflect both immediate and direct vascular actions and also effects secondary to diuresis (volume redistribution). At rest substantial reductions in pulmonary "wedge" pressure (-29%), with a consequent fall in cardiac output (-10%), are described. Total systemic vascular resistance initially increases but "reverse autoregulation" over subsequent weeks returns this elevation gradually towards control values. Tolerance to these initial hemodynamic effects does not occur with maintained therapy; moreover, echocardiographic markers of contractility and exercise capacity may increase. The early venodilator effects of diuretic drugs can be attributed to prostaglandin release and the initial pressor actions to activation of the renin angiotensin system; these vascular actions may have limited relevance to long-term beneficial effects on hemodynamics. Direct pulmonary vasodilation and improved pulmonary compliance remain an interesting finding. Although most patients are both symptomatically and hemodynamically improved at rest, the actions during exercise are more varied. Some individuals with severely impaired left ventricular function show little hemodynamic improvement, whereas those with milder dysfunction usually benefit; in the main this is probably related to the latter being on a steeper cardiac function curve.(ABSTRACT TRUNCATED AT 250 WORDS)

Bumetanide↗
PubMed1993

The place of diuretics in the treatment of hypertension: a historical review of classical experience over 30 years.

Thiazide diuretics have been the mainstay of antihypertensive therapy for over 30 years. Their precise mechanism of antihypertensive action is still incompletely understood. They reduce arterial pressure initially through a fall in plasma volume and cardiac output. However, with chronic administration cardiac output tends to return toward pretreatment levels, suggesting that the long-term pressure reduction is mediated through a reduction in vascular resistance. Although multiple lines of evidence suggest that salt and water loss is an essential part of the mechanism, at least in some cases an indirect vasodilator effect may play a role as well. The antihypertensive efficacy of diuretics is proven; they are at least as effective as other classes of antihypertensive drugs. They have been shown to protect against stroke, but not against mortality from myocardial infarction. There is some concern about the metabolic side effects, such as hypokalemia, hyperglycemia, and hyperlipidemia. In order to minimize these side effects the lowest effective dose should be used. Diuretics are likely to remain first-line antihypertensive agents, but they should be considered as one of several possible choices for the initial therapy among other classes, such as beta-blockers, ACE inhibitors, or calcium entry blockers.

Antihypertensive Agents↗
PubMed1983

[Blood pressure during isometric and dynamic exercise under long-term antihypertensive treatment with beta receptor blockaders and diuretics].

In 34 men with essential hypertension the increase in blood pressure during static and dynamic exercise, after long-term antihypertensive medication, was investigated in a randomized prospective study. The patients were randomized to either hydrochlorothiazide or to atenolol. The exercise tests were performed after a mean treatment duration of 14 months. At this time, the entering blood pressure was significantly and equally lowered from 163/108 to 148/96 mm Hg with a mean dose of 71 mg hydrochlorothiazide and from 164/108 to 147/91 mm Hg with a mean dose of 144 mg atenolol. The heart rate was significantly lower under beta-blocker therapy (62 min-1) than with diuretics (78 min-1). There were no significant differences in the systolic and diastolic blood pressure rise between the two therapy groups during static exercise with the hand grip (33% of the earlier determined individual maximum for 2 min duration) and with the squatting technique (for 2 min). During dynamic exercise on the bicycle ergometer (50-100 W) the increase in the systolic blood pressure was significantly lower between 70 and 100 W, with a range from 12 to 28 mm Hg, in the beta-blocker group than in the diuretic group. There were no differences in diastolic blood pressure between the two therapy groups. Rate-pressure product as a parameter for the myocardial oxygen consumption and heart rate were significant lower in the beta-blocker group as compared with the diuretic group, at rest and during both kinds of exercise and at all exercise steps.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

Prediction of diuretic mobilization of cirrhotic ascites by pretreatment fractional sodium excretion.

In a randomized prospective study the efficacy and side effects of xipamide versus the combination spironolactone/furosemide in the treatment of cirrhotic ascites were studied. Out of 27 patients four responded to a basic treatment consisting of salt and water restriction and one had to be excluded because of deterioration of kidney function. The remaining 22 patients were randomized to additional treatment with either 20 mg xipamide/day (group I) or 200 mg spironolactone/day combined with 40 mg of furosemide every other day (group II). A response to treatment during the first 4 days was seen in 7 of 11 patients of group I versus only 3 of 11 patients in group II. In the latter group 7 of 11 patients finally responded after 8 days of treatment. Responsiveness to either diuretic treatment strongly depended on pretreatment fractional Na excretion, FENa. The resistance to diuretic treatment can be predicted by a FENa less than 0.2%, and could be overcome by additional strategies known to reduce avid proximal Na reabsorption. Xipamide frequently induced hypokalemia, whereas hyperkalemia was seen following treatment with spironolactone/furosemide. Kidney function remained stable during either diuretic treatment.

Adult↗
PubMed1988

Role of diuretics, hormonal derangements, and clinical setting of hyponatremia in medical patients.

Because hyponatremia is frequently associated with preceding diuretic treatment and unrestricted fluid intake--conditions which have not been addressed sufficiently in published literature--we studied the pathophysiology and the clinical setting of such hyponatremia in a large group of internal medicine patients. We observed: a) Of an initial 310 patients with chemical hyponatremia only 204 (64%) had an associated plasma hypoosmolality. Since a normal plasma osmolality excludes a disturbance of water metabolism only the 204 patients with hypoosmolar hyponatremia were included in the study. This data shows that plasma osmolality is an essential measurement in any evaluation of hyponatremia. b) In 204 consecutive patients with hypoosmolar hyponatremia the electrolyte disturbance was related to advanced congestive cardiac failure in 25%, decompensated liver cirrhosis in 18%, volume contraction in 28%, syndrome of inappropriate antidiuretic hormone secretion in 19% and renal insufficiency in 4%. c) Plasma vasopressin was measurable in 90% of the 204 patients. It is known that radioimmunoassays to measure vasopressin fail to reliably detect low concentrations of circulating vasopressin (less than 0.5 pg/ml). It may therefore be stated that hypoosmolar hyponatremia was generally characterized by a failure of antidiuretic hormone suppression. d) Mean daily fluid intake of hyponatremic patients was 2.35 +/- 0.15 l. In the presence of stimulated vasopressin this large a fluid intake is bound to worsen the severity of hyponatremia. e) Of 204 patients 126 were treated with diuretics at the time of study. In these patients hyponatremia worsened during such treatments and was associated with evidence of prerenal azotemia. However there were no significant differences between diuretic-treated and -untreated patients with respect to plasma vasopressin stimulation and amount of fluid intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMedDate not supplied

Pitfalls and limitations of diuretic renography.

We report five pediatric cases that illustrate the methodologic pitfalls and limitations of diuretic renography in suspected ureteropelvic junction obstruction. False-positive studies may be related to such avoidable flaws in methodology as premature diuretic administration, inadequate diuretic dose, and bladder distension, or to recent pyeloplasty. False-negative results may occur despite optimum technique, necessitating a follow-up study for confirmation.

Child, Preschool↗
PubMed1990

Diuretics and cation transport in hypertensive blacks.

Thiazide diuretics are particularly efficacious in the treatment of hypertension in blacks. A number of observations suggest that many hypertensive blacks have features consistent with a status of "corrected" volume expansion. Our studies, as well as those of other investigators, show that the Na,K pump is inhibited in leucocytes and erythrocytes of blacks with essential hypertension. This observation is also consistent with the concept of volume expansion in hypertensive blacks, since the Na,K pump is inhibited in many forms of experimental volume expansion, including the administration of salt in normal humans. We postulate that the efficacy of thiazide diuretics may be related to their ability to stimulate the Na,K pump. We present data obtained in 13 black hypertensive men in whom Na efflux, and Na,K-ATPase in the erythrocyte rose significantly after 7 days of treatment with hydrochlorothiazide, 50 mg/day. Diuretic therapy may indirectly result in reduced intracellular calcium in the vascular smooth muscle.

Benzothiadiazines↗
PubMed2001

Quantitative analysis of infantile ureteropelvic junction obstruction by diuretic renography.

Infantile hydronephrosis detected by ultrasonography poses a clinical dilemma on how to treat the condition. This article reports a retrospective study to evaluate infantile hydronephrosis due to suspected ureteropelvic junction (UPJ) obstruction by means of standardized diuretic renography and to speculate its usefulness for quantitative assessment and management of this condition. Between November 1992 and July 1999, 43 patients who had the disease detected in their fetal or infantile period were submitted to this study. Standardized diuretic renograms were obtained with 99mTc-labeled diethylene-triaminepenta-acetate (Tc-99m-DTPA) or 99mTc-labeled mercaptoacetyl triglycine (Tc-99m-MAG3) as radiopharmaceuticals. Drainage half-time clearance (T 1/2) of the activity at each region of interest set to encompass the entire kidney and the dilated pelvis was used as an index of quantitative analysis of UPJ obstruction. Initial T 1/2s of 32 kidneys with suspected UPJ obstruction were significantly longer than those of 37 without obstruction. T 1/2s of kidneys which had undergone pyeloplasty decreased promptly after surgery whereas those of units followed up without surgery decreased more sluggishly. These findings demonstrate that a standardized diuretic renographic analysis with T 1/2 can reliably assess infantile hydronephrosis with UPJ obstruction and be helpful in making a decision on surgical intervention.

Child, Preschool↗
PubMed1998

Interaction of the diuretics torasemide and U-37883A with the K(ATP) channel in rat isolated aorta.

In this study we have investigated the interaction of the loop diuretics torasemide and furosemide and of the eukalemic diuretic U-37883A (4-morpholinocarboximidine-N-1-adamantyl-N'-cyclohexylhyd rochloride) with the ATP-sensitive K+ channel (K(ATP) channel) in rat aortic rings. Torasemide contains a sulphonylurea group which might enable the compound to interfere with K(ATP) channels; this group is lacking in furosemide. U-37883A blocks several types of K(ATP) channels. The interaction with the vascular K(ATP) channel was probed in binding studies, 86Rb+ efflux experiments and vasorelaxation assays. Torasemide inhibited the binding of the K(ATP) channel inhibitor [3H]glibenclamide and of the opener [3H]P1075 with IC50 values of 19 and 45 microM, respectively; furosemide and U-37883A were inactive or interfered with binding in a nonspecific way. In 86Rb+ efflux experiments, the loop diuretics, at microM concentrations, inhibited basal tracer efflux to 50% whereas U-37883A had no effect. P1075-stimulated 86Rb+ efflux, a qualitative measure of K(ATP) channel opening, was inhibited by U-37883A and torasemide with IC50 values of 0.06 and 130 microM, respectively; furosemide induced only a small (23%) inhibition. In experiments measuring isometric force, torasemide and furosemide partially relaxed endothelium-denuded aortic rings precontracted with noradrenaline or KCl with EC50 values between 6 and 10 microM. The vasorelaxant effect of P1075 was inhibited in a noncompetitive manner by torasemide (300 microM) but unaffected by furosemide. U-37883A increased noradrenaline-induced force and inhibited the vasorelaxant effect of P1075 in an apparently competitive manner with an inhibition constant of 0.4 microM. The data show that torasemide interferes specifically with the binding of the K(ATP) channel modulators [3H]glibenclamide and [3H]P1075 and with the K(ATP) channel opening and vasorelaxant effects of P1075 whereas furosemide is inactive. This suggests that the interaction of torasemide with the vascular K(ATP) channel is due to the sulphonylurea group present in torasemide. U-37883A, which does not inhibit P1075 binding, is one of the most potent blockers of P1075-induced 86Rb+ efflux yet described but is relatively weak as an inhibitor of P1075-mediated vasorelaxation. The opposite vascular actions of torasemide and U-37883A are expected to contribute to the renal effects of these drugs.

Adamantane↗
PubMed2000

Treatment of arterial hypertension with diuretics, beta- and calcium channel blockers in old patients.

Hypertension increases in prevalence with age. Population based studies suggest that more than 50% of people over the age of 65 years may have chronic hypertension. Hypertension, especially systolic hypertension, is the single most common, powerful, however, treatable risk factor for cardiovascular morbidity and mortality in the elderly. In order to assess the effectiveness of antihypertensive drug therapy among the elderly, with diuretics, beta-blockers and calcium channel blockers, a literature search was performed at the Cochrane Library, Medline and Excerpta medica. The Cochrane Hypertension Group identified 14 randomised controlled trials of at least one year duration with 21,785 elderly subjects where diuretics, beta-blockers or calcium channel blockers were used in the treatment group as first line drugs. In their meta-analysis (including one small trial with a central acting antiadrenergic drug) there was a decrease in total mortality (111 vs 129 deaths) and cardiovascular morbidity and mortality (126 vs 177 events) within the treatment group. The three trials restricted to persons with isolated systolic hypertension indicated beneficial effects in the treatment group with regard to cardiovascular morbidity and mortality (104 vs 157 events). Trial data on adverse effects is limited. In three studies, where adverse effects were reported, no substantial differences between treatment and control groups in measures of physical, cognitive and emotional function were found. Cardiovascular benefits of treatment with low dose diuretics or beta-blockers are cleared for elderly subjects with either diastolic or isolated systolic hypertension. Treatment with a long-acting dihydropyridine calcium channel blocker shows beneficial effects in reducing cardiovascular morbidity and mortality for elderly people with isolated systolic hypertension. Due to inconsistent findings in a subgroup meta-analysis of antihypertensive drug treatment in very old people, the efficacy of antihypertensive treatment in these subjects still remains unclear.

Adrenergic beta-Antagonists↗