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PubMed1985

[Therapy of dilated cardiomyopathy with digitalis, diuretics and vasodilators].

The treatment of dilated cardiomyopathy is primarily concerned with that of congestive heart failure. Digitalis is widely use in dilated cardiomyopathy but an improvement in the prognosis has not yet been demonstrated. Furthermore, the effects of digitalis in patients with sinus rhythm are debatable. If dilated cardiomyopathy induces atrial fibrillation and tachyarrhythmia, digitalis should be used. Diuretics are helpful in the treatment of congestive heart failure associated with dilated cardiomyopathy. By reducing hypervolemia and by venous dilatation, diuretics lower preload and afterload. This leads to relief of congestion and termination of the vicious cycle of congestive heart failure. Accordingly, the prognosis of dilated cardiomyopathy might be improved by diuretics. There are numerous diuretics acting differently on the renal tubules, the choice of which depends on the renal function and serum electrolyte concentrations. Reduction of preload and afterload improves congestive heart failure as has been demonstrated repeatedly. Many substances have therefore been used for arterial and venous dilation with differing results. At least for short-term periods, congestion is reduced and cardiac output increases. Especially inhibitors of angiotensin II converting enzyme are very effective since they act both in the arterial and venous systems. Additionally, inhibition of the action of angiotensin may be regarded as causal therapy since the renin-angiotensin system is the trigger for vasoconstriction and fluid retention in congestive heart failure. Unlike other substances, ACE inhibitors have been demonstrated to improve prognosis of patients with congestive heart failure. At present, combined diuretic therapy and angiotensin conversion enzyme inhibition would seem the most reasonable treatment for patients with dilated cardiomyopathy and sinus rhythm. If atrial fibrillation and tachyarrhythmia develop, additional digitalis therapy is effective.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

[Hypokalemia, hypomagnesemia and ventricular arrhythmia during diuretic treatment of arterial hypertension].

Diuretics have been used for 25 years in the treatment of arterial hypertension, where they have proved effective and well tolerated. However, recent therapeutic trials have failed to demonstrate a significant reduction of coronary disease mortality in moderately hypertensive patients under antihypertensive therapy. These disappointing results have led to a reappraisal of the cardiovascular risk inherent in antihypertensive treatments and notably diuretics. Thiazides and the so-called heigh-ceiling diuretics increase urinary potassium excretion, thereby reducing serum potassium levels by 0.3 to 0.6 mmol/l on average. Kalaemia falls below 3.0 mmol/l in 1 to 7 percent of the patients. The long-term consequences of hypokalaemia are imperfectly known. Several authors have used continuous or exertion electrocardiographic recordings to evaluate the risk of ventricular arrhythmia induced by hypokalaemia, but their results are conflicting and inconclusive. The risk of ventricular arrhythmia is perhaps not negligible when hypokalaemia occurs in certain patients with coronary disease or left ventricular hypertrophy who are under digitalis therapy. Diuretics also reduce serum levels of magnesium. The consequences of isolated hypomagnesaemia are obscure. The risk of hyperexcitability seems to be increased when hypokalaemia is associated with digitalis toxicity. The fall in serum concentrations of potassium and magnesium is dose-dependent, and it occurs mainly with the excessive doses formerly prescribed. The dose-response curve of antihypertensive agents is relatively flat, which suggests that diuretics should be used in lower dosage.

Arrhythmias, Cardiac↗
PubMed1988

Erythrocythemia following renal transplantation: influence of diuretic therapy.

Post-transplant erythrocythemia (PTE) is a common finding in renal allograft recipients, although the etiology of this disorder has not been clearly established. We identified 22 patients (9.8%) with PTE from among 225 renal transplant recipients followed for an average of 5.5 years. To characterize possible predisposing factors and to study the clinical significance of PTE, these patients were compared with a control group matched for age, race, sex and etiology of renal failure. Plasma volume (PV) and red blood cell mass (RBCM) were measured in the majority of patients with PTE. Peripheral serum erythropoietin (Ep) levels were determined in the majority of patients in the control and PTE groups. PTE occurred an average of 11.4 months after transplantation. Risk factors for the development of PTE were pretransplant hypertension, retention of native kidneys, higher pretransplant hematocrit, and diuretic use for treatment of post transplant hypertension. Ep levels in the PTE and control groups were not significantly different. Twenty of the 22 patients with PTE were receiving concurrent diuretic therapy, and hematocrits fell to normal levels in all of these patients following cessation or dose reduction of diuretic. No other treatment of PTE was utilized, excluding the phlebotomy of a single unit of blood from one patient. No thromboembolic complications were noted during the follow-up period. We conclude that PTE is frequently induced by overzealous diuretic therapy for treatment of post-transplant hypertension. Discontinuation or reduction of diuretic therapy results in resolution of PTE in nearly all patients. From this experience we have developed an algorithm for the investigation and management of PTE.

Adult↗
PubMed1987

[Cardiovascular risk of diuretics in the treatment of arterial hypertension].

During the last 25 years, diuretics have been widely used with safety and efficacy in the treatment of arterial hypertension and edematous states. Nevertheless, recent intervention trials failed to show a significant decrease in mortality of ischemic heart disease in hypertensive patients given pharmacological treatment. These results led to reassessment of cardiovascular risks of antihypertensive drugs per se and particularly diuretics. Diuretics have a kaliuretic effect and long-term administration decreases serum potassium levels by 0.3 to 0.6 mmol/l. The long-term consequences of hypokaliemia are not well defined. The incidence of hypokaliema-induced ventricular arrhythmias has been studied with exercise or continuous ambulatory electrocardiograms but results are still conflicting. Patients with digitalis treatment, or with preexisting ischemic heart disease or left ventricular hypertrophy may be at high risk for developing ventricular arrhythmias. Glucose intolerance is related in part to the degree of hypokalemia and its incidence decreases with lower dosage of diuretics. Lipid disturbances including hypertriglyceridemia and increase in LDL-cholesterol have not been found to be persistent in long-term administration (1 yr or more) of diuretics.

Arrhythmias, Cardiac↗
PubMed1977

Do diuretics have antihypertensive properties independent of natriuresis?

To ascertain whether diuretics have an antihypertensive effect independent of natriuresis, 12 stable patients on maintenance hemodialysis underwent a crossover evaluation with hydrochlorothiazide, 50 mg daily, metolazone, 5 mg daily, or placebo in 4-wk treatment periods for 6 mo. Compliance was assured by pill counts and serum drug concentrations. All patients had daily urine less than 100 ml. Pre- and postdialysis blood pressure, body weight, plasma volume, and plasma renin activity were monitored. Over the 6-mo study period there were no statistically significant changes in any parameter related to diuretic therapy. It is concluded that a functioning kidney with the ability to respond to diuretics with a natriuresis is necessary for the antihypertensive action of diuretics. Direct vascular effects of diuretics to lower peripheral resistance could not be demonstrated in this unique patient population.

Adult↗
PubMed1988

Renal action of a novel uricosuric diuretic, S-8666. I. Clearance and tubular microinjection studies in rats.

Clearance and tubular microinjection techniques were used to evaluate the effects of a novel uricosuric diuretic, S-8666, on renal function and tubular absorption of urate by the rat kidney. Tubular sites of diuretic action of S-8666 were determined indirectly using osmolar clearance techniques. The i.v. injection of S-8666 at a dose ranging from 0.3 to 3.0 mg caused a dose-dependent increase in urine flow and sodium excretion. Potassium excretion was increased significantly but the increase was not marked as compared with sodium excretion. Glomerular filtration rate was not changed by S-8666. The diuretic response reached a maximum within 5 min and was retained for 45 min with 1 mg of S-8666. The comparison with the effect of furosemide revealed that furosemide was 13 times more potent than S-8666. Both the free water reabsorption on hydropenia and free water clearance in hydrated animals decreased with administration of S-8666. The urinary excretion of urate increased significantly after the administration of S-8666. By contrast, furosemide did not increase urinary excretion of urate. Total urinary urate recovery after S-8666 administration was higher after the microinjection of [14C]urate into early proximal tubule sites. We conclude that S-8666 acts as a uricosuric diuretic agent with the major site of altered urate absorption being in the proximal convoluted tubule and the major site of diuretic action being in the cortical and medullary diluting segments.

Animals↗
PubMed1987

Relationship between metabolism and pharmacologic activity of SQ 27,786, an angiotensin converting enzyme inhibitor with potent diuretic activity.

SQ 27,786 is a sulfhydryl-containing angiotensin converting enzyme (ACE) inhibitor, which also possesses potent diuretic activity in dogs after intravenous administration. The absorption, distribution, metabolism and elimination of 35S-labeled SQ 27,786 was studied in dogs to determine if the observed pharmacologic activities were intrinsic to this compound or the result of metabolism to separate ACE-inhibitory and diuretic moieties. The poor pharmacologic activity observed after oral administration was found to be due to poor absorption of the ACE-inhibitory-diuretic compound. The results of this study indicated that SQ 27,786 was excreted largely intact, either as the parent compound, the symmetrical disulfide of the parent compound, or as mixed disulfides of the parent compound with endogenous sulfhydryl compounds (e.g., SQ 27,786-L-cysteine) in a manner similar to captopril. It was concluded that the observed diuretic and ACE inhibitory activities were the result of intact SQ 27,786 and not of metabolites resulting from cleavage of the molecule to separate diuretic and ACE inhibitory moieties.

Angiotensin II↗
PubMed1987

Volume expansion diuretic renal scan in urinary tract obstruction.

The diuretic renal scan is used to differentiate the obstructed dilated urinary system from the nonobstructed dilated system. The technique, however, has a false-positive and indeterminate rate of 10%-15%. This usually is due to variables such as the degree of dilatation of the pelvicalyceal system or ureter, the degree of bladder distention, the diuretic dose, and the state of hydration. We developed the volume expansion diuretic renal scan (VEDRS) to overcome these variables and to improve the accuracy of the technique. Twelve patients who had obstructive patterns on the diuretic renal scan were evaluated. Ten patients were shown to be dilated but not obstructed. Two patients were confirmed as obstructed. This technique improves the accuracy of the diuretic renal scan.

Adolescent↗
PubMed1987

Diuretic-associated hypomagnesemia in the elderly.

Serum magnesium concentration was measured in 320 consecutive elderly patients (mean age, 81 years) receiving diuretic therapy at the time of hospital admission. When compared with serum concentrations of 250 elderly patients who were not taking diuretics at the time of hospital admission, only the group taking thiazide diuretics had a significantly reduced mean serum level. The 24-hour urine sampling from representative subgroups demonstrated impaired magnesium-conserving ability in hypomagnesemic subjects receiving loop and thiazide diuretic therapy. Patients taking therapy that included a potassium-sparing diuretic had no significant evidence of reduced magnesium-conserving ability. Dietary assessments of the study population revealed suboptimal magnesium intake in the diet.

Aged↗
PubMed1986

Low-dose diuretic therapy for hypertension.

The efficacy of low dosages of diuretics was evaluated in two studies. In one, 62 (48%) of 130 patients became normotensive with 2.5 mg/day of metolazone. In the other, 28 (49%) of 57 patients became normotensive with 25 mg of chlorthalidone, compared with 12 (22%) of 55 patients given placebo. There was a marked variation in blood pressure response and the occurrence of hypokalemia (less than 3.5 mEq/L of potassium) from center to center and within patient groups in both studies. The mean decrease in serum potassium was between 0.5 and 0.6 mEq/L in the metolazone group and 0.44 mEq/L in the chlorthalidone-treated patients. This degree of hypokalemia is only slightly less than that noted when larger dosages of thiazide diuretics are used (0.6 to 0.7 mEq/L). It is concluded that 2.5 mg/day of metolazone or 25 mg/day of chlorthalidone are effective antihypertensive agents but that blood pressure lowering may be inconsistent at these dosage levels. It is reasonable, therefore, to begin diuretic therapy with low dosages, but larger dosages (5 mg of metolazone or 50 mg of chlorthalidone) should be tried before adding another drug or concluding that diuretic therapy is ineffective if an acceptable blood pressure response is not obtained. The degree of hypokalemia that occurs at lower-dose therapy is variable but may be of less clinical significance than that noted with higher dosages of diuretics in some patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Chlorthalidone↗
PubMed1985

Effect of three loop diuretics and prostaglandins E2 & I2 on the isolated perfused rat mesenteric vasculature.

Rat superior mesenteric vascular bed was isolated, perfused by the artery with Krebs solution and the perfusion pressure monitored. Dose-response curves to noradrenaline and KCl administered as bolus doses were obtained. A 1 hr continuous infusion of either piretanide (10 micrograms ml-1) frusemide (40 micrograms ml-1) or bumetanide (2 micrograms ml-1) decreased the sensitivity of the preparation to noradrenaline but not to KCl. This effect was antagonized by flurbiprofen (12 micrograms ml-1) pretreatment. A 1 hr continuous infusion of prostaglandin (PG)E2 increased the sensitivity of the preparation to both noradrenaline and KCl. PGI2 (5 ng bolus) or diuretic perfusion antagonized the responses to noradrenaline but not those to KCl. PGI2 and diuretics in combination further decreased the responsiveness of the preparation to noradrenaline. KCl responses were unaffected by either PGI2 or diuretics, alone or combined. The results suggest that the loop diuretics decrease the responsiveness of the isolated rat superior mesenteric vascular bed preparation to noradrenaline, possibly by increasing the level of PGI2, an effect which may be an important factor in the cardiovascular activity of the diuretics.

Animals↗
PubMed1985

[Diuretics and antihypertensive agents in chronic kidney insufficiency: comparison of the effects of metolazone and furosemide].

Increasing dosages of two potent diuretic agents (5, 10, 20 mg metolazone or 40, 80, 160 mg furosemide) were compared in 35 patients with hypertension and chronic renal failure. In cases with insufficient blood pressure control, 10 mg pindolol was given as a second drug. Finally, patients not responding to a betablocker-diuretic combination received 100 mg hydralazine as a third drug. Both diuretics had comparable antihypertensive potency during a treatment period of up to 12 weeks. Maximal antihypertensive response was observed under 10 mg metolazone or 160 mg furosemide. However, only in 25% of our patients blood pressure was normalized with diuretic monotherapy (metolazone or furosemide). The remaining cases needed either an additional betablocker or a combination of three different antihypertensive agents. Under these conditions a substantial proportion of our patients (20%) did not reach the therapeutic goal (diastolic blood pressure less than 95 mm Hg). These results document the difficulties of hypertension management in chronic renal failure. An early change to the stepped-care approach should be made in all cases with insufficient blood pressure response to potent diuretics.

Adult↗
PubMed1982

Studies on the nature and mechanism of the diuretic activity of the opioid analgesic ethylketocyclazocine.

Subcutaneous injection (0.1 - 3.0 mg/kg) of ethylketocyclazocine (EKC; a prototype kappa agonist) resulted in a dose-dependent increase in urine formation in conscious rats. The increase in urine volume was unaccompanied by a corresponding increase in electrolyte excretion; thus, EKC behaved like a "water diuretic." The diuretic activity was completely abolished by naltrexone, an opiate antagonist. Water loading (10 ml/kg) and EKC (0.5 mg/kg) diminished plasma vasopressin levels equally 60 min after treatment. However, urine formation during the 1 st hr was greater in EKC-treated rats than in water-loaded rats. These results suggested that more than one component was responsible for the diuretic activity of EKC. A central effect of EKC on plasma vasopressin and urine volume was not evident. EKC (10 micrograms/rat) when injected s.c. caused diuresis, but was ineffective as a diuretic when injected into the lateral ventricle. EKC was effective in blocking stimulation of vasopressin secretion caused by volume contraction. EKC also blocked vasopressin-stimulated water flow in the toad bladder, a model of the renal distal tubule and collecting duct. We propose that EKC is diuretic by virtue of inhibition of vasopressin secretion and attenuation of the ADH response in the kidney. Both of these actions may be mediated via opioid receptors responsive to kappa agonists and inaccessible from the cerebroventricle.

Analgesics, Opioid↗
PubMed1984

Mode of action of conventional and potassium-sparing diuretics--aspects with relevance to Mg-sparing effects. Review of the present state of the art and recent findings.

The sites and modes of action of five groups of diuretics within the nephron, and their effects on magnesium excretion are outlined. More than 60% of the glomerularly filtered magnesium is reabsorbed in the loop of Henle. Hence, the loop diuretics induce a strong magnesium excretion. The benzothiadiazine diuretics increase magnesium excretion only moderately. In contrast, the potassium-sparing diuretics amiloride and triamterene, as well as the aldosterone antagonists, increase magnesium reabsorption and therefore may be designated as magnesium-conserving diuretic drugs. The possible modes of action of this property are discussed.

Amiloride↗
PubMed1983

[Various principles of treatment of hypertension with diuretics].

A scheme of prolonged continuous treatment has been developed for patients with essential hypertension (EH). It is based on the principle of differentiated application of the drug in individualized doses, and furosemide testing with subsequent switching to small doses of hypothiazide or some other diuretic agent conducive to the maintenance of the daily natriuresis/mean AP ratio at 1.9-2.0. A series of procedures are also proposed which prevent the development of refractory reaction to the drug or side-effects. The scheme was tested in the course of diuretic treatment of 110 in-patients with EH, stage IIA and IIB, of which 23 were subsequently treated for 6-12 months on an out-patient basis. It was noted that 22% of EH patients were highly sensitive to diuretics, 40-43% showed moderate sensitivity, so that 2-3 weeks' courses of small doses of beta-blockers or corinfar were needed 4-5 times a year to provide a good hypotensive effect, and 38-35% of patients showed poor sensitivity to diuretics and should preferably be treated with other hypotensive agents. The diuretic treatment according to the new regimen was associated with a reduced rate of side-effects.

Adult↗
PubMed1982

Zinc deficiency and the kidney. II. Response of zinc-deficient rats to three diuretic drugs.

Carbonic anhydrase is a zinc metalloenzyme whose activity may be affected by zinc deficiency. This investigation was designed to evaluate the effect of zinc deficiency on the response to three diuretic drugs which vary in their capacity to inhibit carbonic anhydrase: acetazolamide, furosemide and hydrochlorothiazide. The response of the zinc-deficient rats was compared to that of pair-fed and ad libitum zinc-supplemented controls. The pattern of electrolyte excretion by zinc-deficient rats in response to the three diuretics was qualitatively similar to that of the pair-fed and zinc-supplemented rats. When corrected for differences in body weight between the three groups, the natriuretic response to the diuretics in zinc-deficient rats was greater than that of either the pair-fed or zinc-supplemented controls. Although administration of the diuretics increased potassium excretion in all groups, the response of the zinc-deficient rats was attenuated. These differences in the response of zinc-deficient rats to diuretics did not appear to be related to the capacity of these drugs to inhibit carbonic anhydrase.

Acetazolamide↗
PubMed1981

[Therapy of coronary insufficiency with diuretics].

Saluretic drugs like thiazide and benzothiadiazine (chloruretic sulfonamides), potassium-sparing diuretics (amiloride, triamterene and spironolactone) and diuretics with an effect on the loop of Henle (furosemide, ethacrynic acid, bumetadine and etozoline) support the efficiency of digitalis preparations in such cases, in which the load of the heart may be diminished by hemodynamic disburdening of the myocardium through reduction of preload. Here, reduced venous filling pressure is the result of increased elimination of sodium and of dehydration. These drugs are efficacious, but can endanger the patient even if prescribed under right indication and by right dosage. Therefore they should be taken only if necessary and only under continuous medical supervision. The therapeutic breadth of the different diuretics is more favourable than that of the digitalis glycosides. Thus the careful prescription of diuretic drugs can enhance digitalization significantly, especially for patients of higher age with increased sensitiveness on heart glycosides or with supposedly "refractory" heart failure. A rapid intravenous injection of furosemide is the best method for the emergency treatment of an acute pulmonary edema in consequence of left heart failure. This is efficacious in a shorter time and in a better manner than an initial injection of heart glycosides. The favourable effect of diuretic drugs in myocardial failure may be explained by improving the force-velocity curve of the heart with reduction of preload of the myocardium and with diminished venous congestion.

Diuretics↗
PubMed1995

Diuretic activity of N'-disubstituted morpholinoguanidine analogs of U-37883A in rats and dogs.

U-37883A is a K+ sparing diuretic which selectively blocks openers of vascular ATP-sensitive K channels. Many N'-disubstituted morpholinoguanidine (N'-DMG) analogs of U-37883A were synthesized and tested for diuretic activity. In conscious rats, 10-100 mg/kg orally of the most active N'-DMGs increased urine volume (V) and Na+ excretion by up to 4-fold with little kaliuresis. The N'-DMGs U-37997A and U-38658A were less potent than standard diuretics, but did not induce the K+ loss seen with hydrochlorothiazide and furosemide or the K+ retention of amiloride and triamterene. In conscious dogs, 10 mg/kg i.v. of the N'-DMGs U-40389A and U-52090 increased V and Na+ excretion by over 7-fold with little kaliuresis. Despite their attractive diuresis, all of the N'-DMGs had narrow margins of safety. Reflecting their direct myocardial depressant action, in isolated rat hearts, bolus intracoronary U-37883A, U-18177A, and U-38658A (0.25-10 mumol) severely reduced the rate (-10 to -100%) and force (-9 to -100%) of contraction. These studies characterize the eukalemic diuretic activity of N'-DMG analogs of U-37883A, and demonstrate the marked cardiac depression characteristic of the morpholinoguanidine diuretic series.

Adamantane↗