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PubMed1987

Ventricular dysrhythmias in middle-aged hypertensive men treated either with a diuretic agent or a beta-blocker.

The purpose of this study was to identify the frequency of cardiac dysrhythmias in two similar groups of hypertensive middle-aged males (age 45-66). They had previously been randomized either to a diuretic treatment (n = 42), or a beta-blocking agent (n = 41). A 24-hour ambulatory Holter monitoring, and serum potassium, was obtained in all patients, serum magnesium was measured in 35 patients. The mean number of ventricular premature beats (VPBs) and the frequency of complex arrhythmias (19 vs. 5) was significantly higher in the diuretic group (p less than 0.01). The serum potassium was significantly lower (p less than 0.001) in the diuretic group, and there was a significant (p less than 0.005) inverse correlation between the number of VPBs and the serum potassium in all treated patients. The patients with complex arrhythmias were older (p less than 0.01) than the remainder of the patients. No correlation between serum magnesium and VPBs or complex arrhythmias was found. This study demonstrates increased frequency of VPBs in older hypertensive males, treated with diuretics, and that hypokalaemia predisposes to increased cardiac arrhythmias. We conclude that in older mildly hypertensive men hypokalaemia should be avoided.

Aged↗
PubMed1990

Diuretic ultrasound. A non-invasive technique for the assessment of upper tract obstruction.

A study was made of the diagnostic reliability of renal ultrasound with a diuretic in the evaluation of upper tract obstruction. The test comprised an initial renal ultrasound examination followed by the intravenous injection of 250 ml physiological saline with 40 mg frusemide; further ultrasound scans were carried out from 5 to 150 minutes later. A total of 67 patients was studied and the results were compared with those of diuretic intravenous urography, diuretic renography and, in some cases, the Whitaker test. Dynamic ultrasound with a diuretic showed a sensitivity of 94%, specificity of 94%, positive predictive value of 91% (obstructive), negative predictive value of 96% (non-obstruction) and a total diagnostic capacity of 94%.

Adolescent↗
PubMed1993

Effect of tienoxolol, a new diuretic beta-blocking agent, on urinary prostaglandin excretion in the rat.

1. The effects of tienoxolol, (ethyl 2-[3-[(1,1-dimethylethyl)amino]-2-hydroxypropoxy]-5- [(2-thienylcarbonyl) amino] benzoate, hydrochloride), a novel drug exhibiting both diuretic and beta-adrenoceptor blocking properties, were investigated on urinary 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and PGE2 excretion in the rat and compared to those of reference diuretic (furosemide) and beta-adrenoceptor antagonists (acebutolol, propranolol). Since tienoxolol was shown to bind to A1 and A2 adenosine receptors, the action of theophylline was also evaluated. 2. Tienoxolol (8-128 mg kg-1, p.o.) induced a dose-related increase of 6-keto-PGF1 alpha excretion from 32 mg kg-1 but a significant elevation of urinary PGE2 levels was only reached after administration of 128 mg kg-1. However, renal prostaglandin concentrations were not modified by tienoxolol. 3. Furosemide (32 mg kg-1) displayed a strong diuretic activity but did not enhance 6-keto-PGF1 alpha excretion. Likewise, the latter was unaffected by acebutolol and propranolol (128 mg kg-1) and no significant diuresis was observed following administration of these two beta-blocking agents. Theophylline (64 mg kg-1), like tienoxolol, was able to induce both diuresis and urinary prostaglandin excretion. Furthermore, they bound with similar affinities to A1 and A2 adenosine receptors. This led to the suggestion that a relationship between P1-purinoceptors, prostaglandin release, diuresis and natriuresis could exist. 4. Oral co-administration of NECA (0.2 mg kg-1) with tienoxolol markedly reduced the urinary 6-keto-PGF1 alpha excretion observed when tienoxolol was administered alone. However, neither diuresis nor natriuresis were modified, demonstrating that the proposed relationship was untenable. 5. In conclusion, PGI2 probably does not participate in the diuretic and natriuretic activity oftienoxolol. The increase of urinary 6-keto-PGF1alpha excretion may result not only from the haemodynamic properties of the drug but also from the rise of the urinary flow induced by tienoxolol.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Diuretic and saliuretic effects of 1,3-dipropyl-8-cyclopentylxanthine, a selective A1-adenosine receptor antagonist.

We have previously shown that 8-phenyltheophylline (8-PT), a non-selective antagonist at adenosine A1- and A2-receptors, has a diuretic effect. In this study, the diuretic and adenosine antagonist effects of the A1-receptor selective compound 1,3-dipropyl-8-cyclopentylxanthine (CPX) have been examined in the conscious rat. CPX (0.1 and 0.3 mg kg-1 i.v.) significantly attenuated bradycardic but not hypotensive responses evoked by adenosine. In contrast, 8-PT (3 mg kg-1 i.v.) significantly antagonized both adenosine-induced bradycardia and hypotension. CPX (0.1 and 0.3 mg kg-1 i.v.) evoked a dose-related diuretic and saliuretic response in the conscious rat. These results indicate that the diuretic effects of adenosine antagonists are associated with blockade of the A1-receptor sub-type.

Adenosine↗
PubMed1968

The role of left atrial receptors in th diuretic response to left atrial distension.

1. The diuretic response to distension of the whole left atrium caused by obstruction of the mitral orifice has been compared with the effects of distension (by means of small balloons) of the left pulmonary vein/left atrial junctions.2. Distension of the pulmonary vein/atrial junctions caused an increase in heart rate and a diuresis similar to but smaller than that caused by mitral obstruction.3. Section of both ansae subclaviae prevented the increase in heart rate produced by distension of the pulmonary vein/left atrial junctions but had little effect on the diuretic response either to pulmonary vein distension or to mitral obstruction.4. A diuretic response to mitral obstruction could be demonstrated after all nerves from the lungs had been cut but not after the vagus nerves had been cut at levels likely to interrupt the majority of afferent fibres from left atrial receptors.5. The results support the view that stimulation of left atrial receptors is a major factor in the production of a diuretic response to mitral obstruction.

Animals↗
PubMedDate not supplied

Normalization of lipid metabolism after withdrawal from antihypertensive long-term therapy with beta blockers and diuretics.

Blood pressure and serum lipoprotein concentrations were assessed in 40 men with essential hypertension at the end of a long-term, controlled intervention study (HAPPHY) after 5.2 +/- 1.4 years of treatment with hydrochlorothiazide (n = 23) or atenolol (n = 17) and after a wash-out period. After withdrawal from antihypertensive medication, the blood pressures of patients treated with diuretics or beta blockers rose from 142/93 and 145/91 to 159/106 and 165/104 mm Hg, respectively. At the same time, low density lipoprotein cholesterol decreased by 17 and 12 mg/dl, respectively, in the diuretic and beta blocker groups (p less than 0.05). In addition, total cholesterol decreased by 16 mg/dl (p less than 0.05) in the diuretic group, whereas high density lipoprotein cholesterol increased by 8 mg/dl (p less than 0.01) and triglycerides decreased by 27 mg/dl (p less than 0.05) in the beta blocker group at the end of the wash-out period as compared to the final phase of the HAPPHY study. The data indicate the persistence of lipid changes during long-term treatment with hydrochlorothiazide and atenolol. For the first time, it was clearly demonstrated that the well-known unfavorable effects of diuretics and beta blockers on lipid metabolism are reversible after cessation of long-term therapy of several years' duration.

Antihypertensive Agents↗
PubMed1994

Effect of intense angiotensin II suppression on the diuretic response to furosemide during chronic ACE inhibition.

BACKGROUND: Contrary to expectation, most studies have demonstrated that initiation of an angiotensin-converting enzyme (ACE) inhibitor in conventional doses in patients with heart failure reduces the diuretic efficacy of furosemide. Recently, it has been suggested that single low doses (1 mg) but not high doses (25 mg) of captopril enhance furosemide-induced diuresis. It is not known whether the interaction between diuretics and ACE inhibitors are altered during long-term dosing. METHODS AND RESULTS: Eight patients with heart failure treated with diuretics and ACE inhibitors for at least 3 months were studied. All patients were established on captopril 12.5 mg three times daily for 2 weeks before the study. Sodium intake was fixed before the study, and usual medication was withheld on study days. Intravenous furosemide was given on each of 2 study days to maintain a moderate, constant diuresis. Renal plasma flow and glomerular filtration rate (GFR) were determined using clearance techniques, and urine was collected hourly over 4 hours. Captopril 12.5 mg or placebo was given in a randomized, single-blind fashion at the end of the first hour. Compared with placebo, captopril reduced plasma concentrations of angiotensin II (23 +/- 18 versus 4 +/- 3 pg/ml 1 hour after dosing, P < .02) and systolic (131 +/- 31 versus 122 +/- 29 mm Hg, P < .01) and diastolic (74 +/- 15 versus 67 +/- 13 mm Hg, P < .05) blood pressures. GFR fell (55 +/- 24 versus 51 +/- 22 mL/min, P < .02) and effective renal plasma flow rose during the first (198 +/- 76 versus 231 +/- 49 mL/min) and second hours after dosing (185 +/- 69 versus 247 +/- 74 mL/min, P < .02). Similarly, urine volumes, in response to furosemide, increased after captopril (238 +/- 90 versus 283 +/- 111 mL, P < .05, and 245 +/- 78 versus 311 +/- 92 mL, P < .01, 1 and 2 hours after dosing). Urinary electrolyte concentrations fell, but total urinary sodium (22 +/- 7 versus 28 +/- 12 mmol/hr, P < .01) and chloride (20 +/- 6 versus 25 +/- 11 mmol/hr, P < .05) excretion increased in the 2 hours after dosing, as did fractional excretion of sodium (urinary sodium/urinary creatinine) (61 +/- 27 versus 75 +/- 36 mmol/mumol, P < .01). CONCLUSIONS: Intense although transient ACE inhibition with captopril enhances the diuretic effects of furosemide during long-term ACE inhibition.

Aged↗
PubMed1994

Block of IKs, the slow component of the delayed rectifier K+ current, by the diuretic agent indapamide in guinea pig myocytes.

There is a high incidence of diuretic use among patients who develop exaggerated QT prolongation and polymorphic ventricular tachycardia (torsade de pointes) during treatment with action potential-prolonging agents. Diuretic-induced hypokalemia is thought to be the usual mechanism, but a direct effect of diuretic drugs on repolarizing currents is an additional possibility. Therefore, in this study, we examined the effects of the diuretic agents chlorthalidone and indapamide on the cardiac delayed rectifier current. In guinea pig ventricular myocytes, this current is made up of two components: IKr, a rapidly activating, inwardly rectifying current blocked by most action potential-prolonging antiarrhythmics, and IKs, a slowly activating component. In this preparation, indapamide blocked outward current in a time-, voltage- and concentration-dependent fashion, whereas chlorthalidone (1 mmol/L) was without effect. The following features of the effect of indapamide strongly suggest selective block of IKs: (1) Indapamide block was significantly greater with 5000-millisecond activating pulses (-43 +/- 5% at +50 mV [100 mumol/L indapamide]) than with 225-millisecond ones (-20 +/- 5%; n = 5, P < .01), and the signature of the indapamide-sensitive current was a slowly activating delayed rectifier current. (2) The voltage dependence of indapamide block (EC50, 101 mumol/L at +50 mV and 196 mumol/L at +10 mV) was consistent with preferential block of IKs relative to IKr. (3) In the presence of indapamide, an envelope-of-tails test for IKr was satisfied. The drug-insensitive current had rectifying properties similar to those described for IKr in these cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1975

The pathogenesis of post-obstructive diuresis. The role of circulating natriuretic and diuretic factors, including urea.

To investigate the pathogenesis of post-obstructive diuresis, a state of functional "anuria" during ureteral obstruction was created in awake rats by (a) bilateral obstruction (BO); (b) unilateral obstruction and contralateral nephrectomy (UO-Nx); or (c) unilateral obstruction and continuous i.v. reinfusion of urine from the intact contralateral kidney (UO-reinf). These groups were compared with unilaterally obstructed (UO) and sham-operated control (sham) rats. After release of obstruction of 24 h duration, mean urine flows (V) and sodium excretion rates (UNaV) were significantly elevated above those of sham rats in BO, UO-Nx, and UO-reinf animals, but slightly decreased in UO rats. Glomerular filtration rates were comparably depressed in UO, BO, UO-Nx, and UO-reinf rats. These results suggest that post-obstructive diuresis is due to one or more circulating diuretic factors that are normally excreted in the urine, and which, when retained )as in BO or UO-Nx rats) or returned to the circulation (as in UO-reinf rats), exert a diuretic affect. In additional experiments, UO rats infused with urea exhibited post-obstructive diuresis, if extracellular volume contraction was prevented. This result suggests that urea may be an important diuretic factor in post-obstructive diuresis, but does not exclude possible roles for other humoral factors. The intact kidney of UO-reinf rats displayed a massive unilateral diuresis and natriuresis, further suggesting the presence of potent diuretic factors in the urine. A marked increase in the fractional excretion of glomerular filtrate (V/GFR) by the intact kidney suggests that this diuresis may be attributable, in part, to impaired proximal reabsorption.

Aminohippuric Acids↗
PubMed1976

Effects of diuretics on lipid metabolism in patients with essential hypertension.

Available clinical evidence indicates a high prevalence of hyperuricemia in patients with essential hypertension; this becomes accentuated with diuretic therapy. Since there is an association of hyperlipidemia with hyperuricuria and hypertension and since hyperuricemia is a feature of diuretic therapy, we explored whether these relationships might be provoked by prolonged diuretic therapy. Eighteen male patients with uncomplicated essential hypertension of mild severity were treated for 9 months with hydrochlorothiazide and supplemental potassium chloride, 100 mg and 45 mEq/day, respectively. Arterial pressure, renal function, and serum electrolyte, uric acid, blood glucose, and lipid concentrations were measured several times before and during therapy. Arterial pressure remained significantly reduced during therapy (P less than 0.001); this was associated with reduced serum potassium (P less than 0.01) and increased blood glucose and serum uric acid concentrations (P less than 0.005, P less than .025, respectively). Blood urea nitrogen, serum creatinine, sodium, cholesterol and triglyceride levels did not significantly change with treatment. Thus, although diuretics increase serum uric acid and blood glucose, their effect on serum lipid concentration is negligible.

Adult↗
PubMed2006

Distribution, activity and evidence for the release of an anti-diuretic peptide in the kissing bug Rhodnius prolixus.

In the haematophagous insect Rhodnius prolixus, diuresis is accomplished through the combined actions of peptidergic diuretic hormones and 5-HT released from neurohaemal sites on the abdominal nerves. Preliminary work on anti-diuresis in this blood-feeder, previously believed to occur through a decrease in the levels of the diuretic factors, indicates that an anti-diuretic hormone, with properties similar to CAP2b (pELYAFPRVamide; recently renamed Mas-CAPA-1), might also be present in R. prolixus. Here, we present evidence from immunohistochemical analysis that suggests a PRXamide-like neuropeptide may be released from the abdominal neurohaemal sites beginning 3-4 h following feeding; a time that coincides with the cessation of diuresis. We also show evidence for an endogenous factor, isolated from the central nervous system using reversed-phase high performance liquid chromatography, which mimics the effects of Mas-CAPA-1. Specifically, this endogenous anti-diuretic factor inhibits rates of 5-HT-stimulated secretion in a dose-dependent manner and elevates intracellular cGMP levels of Malpighian tubules stimulated with 5-HT.

Animals↗
PubMed1994

THE EFFECTS OF ACHETA DIURETIC PEPTIDE ON ISOLATED MALPIGHIAN TUBULES FROM THE HOUSE CRICKET ACHETA DOMESTICUS

Acheta diuretic peptide (Acheta-DP) is a corticotropin-releasing factor (CRF)-related peptide found in head extracts of the house cricket Acheta domesticus. The peptide causes a dose-dependent increase in fluid secretion by cricket Malpighian tubules isolated in vitro, and the apparent EC50 is 1.3 nmol l-1, which is within the physiological range for a peptide hormone. The CRF antagonist alpha-helical CRF(9-41) blocks the action of Acheta-DP in a dose-dependent manner, and the IC50 is estimated to be in the micromolar range. Addition of Acheta-DP to isolated Malpighian tubules is followed by a rapid and marked increase in the level of intracellular cyclic AMP. This precedes any change in voltage or fluid secretion, which strongly suggests that cyclic AMP is the intracellular mediator of Acheta-DP activity. Consistent with this, diuretic activity is potentiated by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, and there is a close relationship between the dose&shy;response curves for cyclic AMP production and for fluid secretion. However, exogenous 8-bromo-cyclic AMP does not mimic all the effects of Acheta-DP, and the peptide may have a dual action on isolated tubules. Fluid secretion by tubules dosed repeatedly with Acheta-DP returns to near basal levels after 3&shy;5 h. This cannot be explained by degradation of the peptide, but might be due in part to oxygen and/or metabolite deficiency. However, tubules that are refractory to Acheta-DP can be stimulated by forskolin, 8-bromo-cyclic AMP and extracts of corpora cardiaca, which is indicative of a homologous desensitization of membrane receptors for the diuretic peptide. Differences in the rate of secretion by morphologically distinct regions of cricket Malpighian tubules have been assessed. In unstimulated tubules, the rate of secretion per unit length by the short distal segment is about twice that of the main tubule. However, diuretic peptides (Acheta-DP and achetakinin-I) have little effect on distal tubule secretion, but evoke a two- to fourfold increase in fluid secretion by the main tubule segment.

Journal Article↗
PubMed1988

Increased diuretic response to furosemide in rats with glycerol-induced acute renal failure.

To clarify the diuretic response to furosemide in a diseased state, the urinary excretion of furosemide, water, and electrolytes was examined after a single intravenous injection of furosemide in control rats and rats with mild acute renal failure (ARF) induced by glycerol. The urinary recovery of furosemide was similar in the control and ARF rats. However, the diuretic response to furosemide was increased in ARF rats compared with control rats. Although the relationship between the urine flow rate (UFR) and the urinary excretion rate of (Na+ + K+) (UV Na + K) was the same in both groups, the urinary excretion rate of K+ (UV K) was decreased in ARF rats. The concentrating ability in ARF rats was also decreased compared with that in control rats. By infusion of aldosterone in ARF rats, both UV K and the concentrating ability were increased and the diuretic response to furosemide was decreased, whereas the relationship between UFR and UV Na + K was not changed. Therefore, it is concluded that the increased diuretic response to urinary excretion of furosemide in ARF rats may be caused, at least in part, by the decreased concentrating ability along the nephron.

Acute Kidney Injury↗
PubMed1991

Studies on uricosuric diuretics. II. Substituted 7,8-dihydrofuro[2,3-g]-1,2-benzisoxazole-7-carboxylic acids and 7,8-dihydrofuro[2,3-g]benzoxazole-7-carboxylic acids.

A series of substituted 7,8-dihydrofuro[2,3-g]-1,2-benzisoxazole-7-carboxylic acids 9 and 7,8-dihydrofuro[2,3-g]benzoxazole-7-carboxylic acids 12 were synthesized and evaluated for uricosuric and diuretic activities in rats. Many of the benzisoxazole derivatives 9 showed uricosuric and only weak diuretic activities, whereas the benzoxazoles 12 exhibited potent diuretic activities with little affecting urate excretion. Among these compounds, 5-chloro-7,8-dihydro-3-phenylfuro[2,3-g]-1,2-benzisoxazole-7-carbo xylic acid (9b, AA-193) was found to be a potent uricosuric agent without diuretic activity and was selected for further development.

Animals↗
PubMed1987

Captopril attenuates diuretic and natriuretic actions of furosemide but not atrial natriuretic peptide.

Atrial Natriuretic Peptide (ANP) exerts a potent diuretic and natriuretic action in rat, dog and man. To test whether these actions of ANP are due to antagonism of the antinatriuretic actions of endogenous angiotensin II, an examination was made of the renal actions of ANP in anesthetized rats with and without captopril pretreatment. Captopril treatment did not alter the diuretic and natriuretic action of a single, intravenous bolus injection of ANP (1000 ng of the 8-33 ANP). Captopril treatment did significantly attenuate the diuretic and natriuretic actions of Furosemide (20 mg/kg ip). This attenuation was not reversed by concomitant, exogenous angiotensin II infusion. These results suggest that while ANP exerts its renal actions independently of the circulating renin-angiotensin system the diuretic and natriuretic action of Furosemide is modulated by a substrate of angiotensin converting enzyme.

Angiotensin II↗
PubMed1991

Loop diuretics for chronic renal insufficiency: a continuous infusion is more efficacious than bolus therapy.

OBJECTIVE: To test the hypothesis that a continuous, low-dose infusion of a loop diuretic is more efficacious and better tolerated than conventional intermittent bolus therapy in patients with severe chronic renal insufficiency (CRI). DESIGN: Randomized, crossover clinical trial with subjects serving as their own controls. SETTING: The General Clinical Research Center of Indiana University Hospital, Indianapolis, Indiana. PATIENTS: Eight adult volunteers with severe stable CRI (mean creatinine clearance, 0.28 mL/s; range, 0.15 to 0.47 mL/s) were recruited from the outpatient nephrology clinics of Indiana University Medical Center. INTERVENTIONS: On admission, diuretic drugs were withdrawn and patients were equilibrated on an 80 mmol/d sodium, 60 mmol/d potassium metabolic diet. Patients were randomized to receive a 12-mg intravenous dose of bumetanide given either as two 6-mg bolus doses separated by 6 hours or as the same total dose administered as a 12-hour continuous infusion. When sodium balance was re-established, each patient was crossed over to the alternative study limb. All patients completed both phases of the study. MEASUREMENTS AND RESULTS: Comparable amounts of bumetanide appeared in the urine during the study period (infusion, 912 +/- 428 micrograms; bolus, 944 +/- 421 micrograms; difference, 32 micrograms; 95% CI, -16 micrograms to 80 micrograms, P = 0.16). The continuous infusion resulted in significantly greater net sodium excretion (infusion, 236 +/- 77 mmol; bolus, 188 +/- 50 mmol; difference, 48 mmol; CI, 16 mmol to 80 mmol, P = 0.01). No patient had episodes of drug-induced myalgias during the continuous infusion compared with 3 of 8 patients with bolus therapy. CONCLUSIONS: In patients with severe CRI, a continuous intravenous infusion of bumetanide is more effective and less toxic than conventional intermittent bolus therapy. Continuous administration will probably be useful in patients with severe CRI who have not achieved an adequate natriuresis or who show evidence of drug toxicity with standard diuretic dosing regimens. A similar benefit may occur in selected diuretic-resistant patients with cardiac or hepatic disease, and studies in these patients seem warranted.

Adult↗
PubMed1976

[Clinical use of pterofen as a diuretic agent in circulatory insufficiency].

Clinical and laboratory observations were conducted using a new Soviet-made drug Pterophene as a diuretic in 30 patients with circulatory insufficiency. Stage IIB and III. Pterophene was found to produce a distinct natriuretuc and diuretic effect. With its daily intake, the effect has a prompt onset, it increases by the 3rd-4th day of therapy, persists for a long period, slightly decreasing in its potency by the 7th-10th day of its continuous administration. A valuable property of Pterophene is its potassium-retaining effect. The drug is well tolerated by the patients, and it can be combined with other diuretics. Pherophene potentiates the diuretic and natriuretic effect of Hypothiaside, Furosemide and Nuvorite, and decreases potassium excretion that was enhanced by these drugs.

Adult↗
PubMedDate not supplied

[Mechanism of the diuretic effect of eufillin].

In acute experiments on rats the xanthine diuretic euphylline did not block the short-circuited current in the proximal tubule, nor did it lower the transtubular potential and the transepithelial resistance of the nephron wall. The diuretic speeded up significantly the passage of the tubular fluid along the proximal region of the nephron and Henle's loop. The dihydroergotoxin and inderal blocking of adrenoreceptors did not produce any influence on the renal effects of the xanthine agent. Reserpine totally blocked the diuretic and saluretic effects of euphylline, whereas other sympatholytics, such as alpha-methyl-dofa, anthabus and hemedin, did not modify the action of the diuretic.

Aminophylline↗