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PubMed1991

Isolation and identification of a new diuretic peptide from the tobacco hornworm, Manduca sexta.

A 30-amino acid diuretic peptide was isolated from the corpora cardiaca-corpora allata complexes and, separately, from medial neurosecretory cells of the Sphingid moth, Manduca sexta. The peptide was found to have the following sequence, determined by automated Edman degradation and mass spectrometry: SFSVNPAVDILQHRYMEKV AQNNRNFLNRV-NH2. We have named the peptide Mas-DP II. The peptide was synthesized and shown to possess diuretic activity in decapitated moths. Mas-DP II is related by sequence homology to a 41-amino acid diuretic peptide identified previously from M. sexta, and it belongs to the family of corticotropin releasing factor-like peptides.

Amino Acid Sequence↗
PubMed1987

Altered furosemide pharmacokinetics in chronic alcoholic liver disease with ascites contributes to diuretic resistance.

Some patients with chronic alcoholic liver disease and ascites have an impaired natriuretic response to furosemide. To elucidate the mechanism of this diuretic resistance, we measured para-aminohippurate and inulin clearances and urinary excretion of electrolytes, prostaglandin E2, and furosemide after intravenous administration of 80 mg of furosemide in 26 patients. The natriuretic response was variable (3.3-172 mEq/h) and was unrelated to basal sodium excretion, renal clearances, or urinary prostaglandin E2. Natriuresis correlated negatively with plasma aldosterone (r = -0.54, p less than 0.01), and strongly with urinary furosemide (range 5.5-76 mg/h, r = 0.71, p less than 0.001). As urinary furosemide excretion reflects the amount of furosemide reaching the active site on the luminal side of the tubule, the data demonstrate markedly reduced amounts of furosemide at its primary site of action in patients with diuretic resistance. Plasma furosemide was higher in patients with reduced furosemide excretion and impaired natriuresis, suggesting that the defect was an impairment of furosemide transport into the tubule. Thus, a major factor in diuretic resistance is altered furosemide pharmacokinetics.

Dinoprostone↗
PubMed1985

Compartment pressure following leg injury: the effect of diuretic treatment.

Acute ischaemia in the tibial compartments is a recognized complication of fractures, vascular injury, vascular surgery, crush injuries and burns. The tissue pressure was measured in the first week after injury and the effect of diuretics has been evaluated in a double-blind randomized manner. The pressure in the anterior tibial compartment was measured in the first week after injury in a double-blind randomized manner in 40 patients who had sustained either accidental or surgical injury of the leg. The pressure in the group treated with placebos increased by 20 per cent in the first 24 hours, whereas the pressure fell by 25 per cent in those treated with diuretics. Diuretic treatment is recommended for patients with injury of the lower limbs.

Adolescent↗
PubMed1991

Loop diuretics block calcium currents in cardiac cells.

Loop diuretics are widely used drugs; serving to alleviate congestive heart failure and hypertension. Their mechanism of action is considered to be an inhibition of sodium retention in the kidneys, by a block of the Na/K/Cl cotransporter. The ensuing natriuresis and diuresis reduces blood pressure and alleviates congestive heart failure. Several earlier reports suggested direct cardiovascular effects, partly preceding the onset of diuresis. In the present study, evidence is presented for a direct action of two loop diuretic agents, bumetanide and furosemide, on cardiac L-type calcium currents in rabbit ventricular and atrial myocytes. This current is reversibly reduced by micromolar concentrations of these drugs. The onset of this effect can be observed within 1-2s, which could indicate a direct action on the calcium channel, independent of secondary effects subsequent to inhibition of the cotransporter. Thus, part of the therapeutic effects of the loop diuretics may be achieved through a direct reduction of cardiac output.

Animals↗
PubMed1980

Increased serum low-density lipoprotein cholesterol in men treated short-term with the diuretic chlorthalidone.

The effect of the diuretic chlorthalidone (100 mg/day for 6 weeks) on serum lipoproteins was evaluated in 37 subjects. In 19 men with essential hypertension (aged 41 +/- 3 yr), 8 normal men (26 +/- 3 yr), or all of these men considered together, chlorthalidone significantly increased serum low density lipoprotein--cholesterol (LDL-C) by 20% (p less than 0.05 to less than 0.01). There was also a tendency for increased LDL-C in seven postmenopausal women (+/- 15%) but not in three premenopausal women with essential hypertension. High density lipoprotein--cholesterol was not significantly changed in hypertensive women or normal men and decreased slightly (p less than 0.05) in hypertensive men. Apolipoproteins A-I, A-II, and B were not changed significantly in women or men. Diuretic-induced lipoprotein alterations were not associated with altered plasma volume and unrelated to variations in serum potassium, glucose, insulin levels, blood pressure, and body weight. Short-term diuretic therapy with chlorthalidone may increase serum LDL-C in young or middle-aged men with normal or high blood pressure.

Adolescent↗
PubMed1991

Posture determines the nature of the interaction between angiotensin converting enzyme inhibitors and loop diuretics in patients with chronic cardiac failure.

The effects of inhibition of the renin angiotensin aldosterone system on the natriuretic and diuretic actions of an intravenous dose of frusemide 40 mg in patients with chronic cardiac failure maintained on oral diuretics were studied in the supine and erect positions. In the patients studied in the supine position the total 4 hour diuresis was decreased from 995 (92) ml to 668 (66) ml and the total 4 hour natriuresis fell from 105 (14) mmol to 67 (14) mmol following the administration of captopril. Creatinine clearance fell from 87 (8) ml/minute to 52 (15) ml/minute. In the patients studied in the erect position the total 4 hour diuresis was 596 (87) ml without captopril and 562 (83) ml with captopril. Total 4 hour natriuresis was 71 (13) mmol without captopril and 65 (9) mmol with captopril. Creatinine clearance was reduced by captopril from 82 (7) ml/minute to 47 (12) ml/minute. The reduction in the diuretic and natriuretic response to frusemide caused by captopril in the supine position is mediated through a fall in glomerular filtration rate. However, in the erect position, which is associated with even further increases in activity of the renin angiotensin aldosterone system, the reduction in diuresis and natriuresis that a fall in glomerular filtration rate would cause is offset by abolition of the rise in sodium retaining hormones, angiotensin II and aldosterone that mediate the antinatriuretic effect of the erect position.

Aged↗
PubMed1985

The effect of loop diuretics upon summating potentials in the guinea pig.

Ototoxic diuretics, ethacrynic acid (50 mg/kg) and furosemide (80 mg/kg) were injected intravenously in guinea pigs. Cochlear microphonics (CM), summating potentials (SPs) and endocochlear potential (EP) were recorded with a microelectrode in scala media of the second turn. CM changes after the injection were comparable with changes in the EP: an initial decrease was followed by an increase which was significantly slower in the case of the ethacrynic acid. SP changes following either diuretic were different from the CM and EP changes. In the first phase, roughly corresponding with the EP decrease to negative values, all SPs irrespective of the original polarity, attained high positive values. The high positive SPs then decreased and 12-18 min after injection reversed polarity. In the late phase all sounds evoked high negative SPs. Approximately 90 min after injection of furosemide normal SPs were again recorded. The return of SPs to control values was very slow after ethacrynic acid; even 140 min after injection the SPs were abnormal. The observed changes in the SPs were compared with those found during asphyxia and anoxia and are considered to result from diuretic effects on the inner and outer hair cells.

Animals↗
PubMed1992

Effects of diuretic therapy on the development of tolerance during continuous therapy with nitroglycerin.

OBJECTIVES: This study examined the effects of concurrent diuretic therapy on the hemodynamic responses to short-term and sustained therapy with transdermal nitroglycerin. BACKGROUND: Sodium retention and plasma volume expansion occur during therapy with nitroglycerin and may play a role in the loss of nitroglycerin effects during sustained therapy. METHODS: Twenty-two normal male volunteers were treated for 1 week with either hydrochlorothiazide and amiloride (50 + 5 mg) (n = 11) or placebo (n = 11) in a randomized, double-blind fashion. All 22 subjects then received continuous transdermal nitroglycerin (19 +/- 1 mg/24 h) for 5 to 7 days. RESULTS: On the first and last day of transdermal nitroglycerin therapy, standing heart rate, systolic blood pressure and hematocrit values were assessed at 8, 9 and 10 AM and 12 noon. Heart rate and blood pressure responses to sublingual nitroglycerin (0.6 mg) were also evaluated before and after sustained transdermal nitroglycerin therapy. A significant loss of the hemodynamic effects of transdermal and sublingual nitroglycerin occurred during sustained therapy in both the diuretic and placebo therapy groups. In both groups, transdermal nitroglycerin therapy was associated with a significant decrease in hematocrit that persisted for the entire treatment period. CONCLUSIONS: These results suggest that diuretic therapy does not prevent plasma volume expansion or the loss of hemodynamic effects during sustained transdermal nitroglycerin therapy. The persistent decrease in hematocrit suggests that plasma volume expansion plays a role in the attenuation of nitrate effects. It also provides evidence of continued vascular activity of nitroglycerin despite loss of systemic hemodynamic effects.

Administration, Cutaneous↗
PubMed1995

Cortisol metabolism in hypertensive patients who do and do not develop hypokalemia from diuretics.

Deficiency of 11 beta-hydroxysteroid dehydrogenase causes hypertension and hypokalemia. To test whether hypertensive patients who develop hypokalemia when treated with diuretics have low levels of activity of this enzyme as a metabolic predisposition to the development of hypokalemia, we measured urinary cortisone, cortisol, tetrahydrocortisol, tetrahydrocortisone, and creatinine in 42 hypertensive patients who either did or did not become hypokalemic on hydrochlorothiazide. The mean ratios of cortisone to cortisol, tetrahydrocortisone to tetrahydrocortisol, tetrahydrocortisol to cortisol, and cortisol to creatinine did not differ between the two groups. We conclude that hypertensives who develop hypokalemia on diuretics do not have low activity of this enzyme. They also do not appear to have low ring A reduction or higher cortisol secretion rates compared with hypertensives who do not develop hypokalemia. We failed to find a metabolic predisposition to the development of hypokalemia by diuretic treatment.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2005

Different effects of long- and short-acting loop diuretics on survival rate in Dahl high-salt heart failure model rats.

OBJECTIVES: We compared therapeutic effects of furosemide, a short-acting loop diuretic, and azosemide, a long-acting one, in hypertensive heart failure rats to test the hypothesis that long-acting diuretics are superior to short-acting types in heart failure. METHODS: Dahl salt-sensitive rats fed an 8% NaCl diet from age 8 weeks were divided at age 21 weeks (compensated hypertrophic stage) into three groups: rats treated with furosemide (40 mg/kg/day), those treated with azosemide (80 mg/kg/day) and untreated rats. Rats fed a 0.3% NaCl diet served as controls. RESULTS: Both medications prevented left ventricular systolic dysfunction and enlargement at age 31 weeks, and attenuated macrophage infiltration, reactive oxygen species generation, and gelatinolytic activity to the same degree. Azosemide suppressed left ventricular fibrosis to the control level, but furosemide did not. Azosemide ameliorated myocardial catecholamine depletion and improved survival rate. Furosemide increased plasma norepinephrine levels and did not exert such beneficial effects. CONCLUSIONS: Azosemide provided better prognosis in heart failure rats compared with furosemide, partly through attenuation of the reflex increase in cardiac sympathetic neuronal activity caused by the development of heart failure. The current findings suggest a need for clinical trials examining whether long- and short-acting diuretics provide a different prognosis in patients with heart failure.

Animals↗
PubMed1995

Thiamin status, diuretic medications, and the management of congestive heart failure.

OBJECTIVE: To assess the prevalence of thiamin deficiency in patients with congestive heart failure who are treated with diuretics that inhibit sodium and chloride reabsorption in the thick ascending limb of the loop of Henle (loop diuretic therapy). DESIGN: A cross-sectional investigation of thiamin status of consecutive patients with congestive heart failure being treated with loop diuretic therapy. SETTING: Cardiology clinic of a midwestern tertiary-care medical center. SUBJECTS: Thirty-eight patients were recruited (mean age +/- standard deviation = 55 +/- 14 years). Validation of methodology was conducted with nine age-matched control subjects. MAIN OUTCOME MEASURES: Thiamin status was assessed biochemically by in vitro erythrocyte transketolase activity assay. Assessment of dietary intake of thiamin was accomplished with a semiquantitative food frequency questionnaire. STATISTICAL ANALYSES PERFORMED: Fisher's exact test and logistic regression were used to evaluate relationships between thiamin status and variables of interest. RESULTS: Biochemical evidence of thiamin deficiency was found in 8 of 38 (21%) patients. Evidence of risk for dietary thiamin inadequacy was found in 10 of 38 patients (25%). Seven of the 8 patients with biochemical evidence of thiamin deficiency met study criteria for dietary adequacy, although quantified data suggested that only 4 of the patients achieved two thirds of the Recommended Dietary Allowance. Biochemical evidence of thiamin deficiency tended to be more common among patients with poor left ventricular ejection fractions (P = .07). CONCLUSIONS: Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk.

Adult↗
PubMed2002

Diuretic and myotropic activities of N-terminal truncated analogs of Musca domestica kinin neuropeptide.

Musca kinin (Musdo-K; NTVVLGKKQRFHSWG-NH(2)) and N-terminal truncated analogs of 4-14 residues in length were assayed for diuretic and myotropic activity on housefly Malpighian tubules and hindgut, respectively. The pentapeptide was the minimum sequence required for biological activity, but it was > 5 orders of magnitude less potent than the intact peptide. The pharmacological profiles of the different analogs in the two assays were very similar, suggesting the same receptor is present on both tissues. Potency was little affected by the deletion of Asn(1), but was reduced > 10-fold after the removal of Thr(2). Deletion of the next 5 residues had relatively little effect, but after the second lysyl residue (Lys(8)) was removed potency fell by one to two orders of magnitude. There was a similar drop in potency after the removal of Arg(10), and at 100 microM the pentapeptide had only 20% of the diuretic activity of the intact peptide. The importance of Arg(10) was confirmed by comparing dose-response curves for Musdo-K [6-15] and Acheta kinin-V (AFSHWG-NH(2)) in the diuretic assay; the substitution of arginine by alanine produced a significant reduction in potency and some loss of activity.

Animals↗
PubMed2000

[Diuretic renography in the diagnostic approach of prenatal hydronephrosis].

OBJECTIVE: To verify the utility of diuretic renography using 99mTc-MAG3 in the evaluation of the urinary tract obstruction in patients with prenatal diagnosis of hydronephrosis. In a neonate with upper urinary tract dilatation, it is difficult to differentiate a true obstruction from a dilated non-obstructed system. MATERIAL AND METHODS: The retrospective study (january 1993-december 1998) included 40 consecutive patients selected from 181 newborns with a prenatal diagnosis of hydronephrosis. The mean age of the performance of the first renography was 2.6 months. RESULTS: The final diagnosis (once the vesicoureteral reflux was ruled out) was: ureteropelvic junction obstruction (UPJ) 16, megaureter 15, ureterocele 3 and stasis 6. Conservative treatment was applied in most of the patients. Nevertheless, 17 of them needed surgical treatment due to the high risk of the permanent renal damage. CONCLUSIONS: 1) UPJ is the most frequent cause of neonatal hydronephrosis (NH) and consequently, of the request for diuretic renographies. The renography with 99mTc-MAG3 has the greatest influence in the therapeutic decision (identifying who should be operated on and when this should be done), due to the fact that it is the disease with the highest rate of surgical interventions. 2). The surgical indication in NH is based on the diuretic renography parameters and/or on the presence of symptomatology. In our series of surgical patients, none of those who had a differential renal function <20% with regard to the contralateral one showed recuperation after surgery (control 6 months later).

Diuresis↗
PubMed1989

1-(2-aminoethyl)-6-aryl-4H- [1,2,4]triazolo[4,3-a][1,4]benzodiazepines with diuretic and natriuretic activity.

A series of 1-(2-amino-1-phenylethyl)-6-phenyl-4H- [1,2,4]triazolo[4,3-a][1,4]benzodiazepines was prepared and evaluated for diuretic activity. These compounds have diuretic and natriuretic activity but no kaliuretic activity when evaluated by oral administration to the conscious rat. The structure requirements for this activity are discussed. In particular it was found that the 2-aminoethyl side chain at C-1 with hydrogen or methyl substituents on the amino group was required for diuretic activity. A substituent at C-8 was also required; soft substituents such as methylthio and iodo at this position favored activity. Compounds with both phenyl and 2-pyridyl substituents at C-6 were active; substituents on the C-6 phenyl, however, reduced or eliminated the activity. Substituents other than phenyl at the 1-position of the 2-aminoethyl side chain were detrimental to activity; phenyl substitution at this position was required for activity when the substituent at C-8 was chloro but not when it was bromo.

Animals↗
PubMed1999

Preparation, purification, and characterization of a reversibly lipidized desmopressin with potentiated anti-diuretic activity.

PURPOSE: . To prepare and characterize a reversibly lipidized dipalmitoyl desmopressin (DPP), and to compare its anti-diuretic efficacy and biodistribution with that of unmodified desmopressin (DDAVP). METHODS: Dithiothreitol (DTT) was used to reduce the intramolecular disulfide bond in DDAVP, and the reduced DDAVP was treated with a thiopyridine-containing disulfide lipidization reagent, Pal-CPD. The product, DPP, was purified by acid precipitation and, subsequently, by size-exclusion chromatography. Reversed-phase HPLC was used to analyze the purity and to evaluate the hydrophobicity of the product. Mass spectrometry was employed to characterize its molecular structure. The biological activity of DPP was demonstrated by the antidiuretic effects in vasopressin-deficient Brattleboro rats. Preliminary pharmacokinetic and biodistribution studies of intravenously injected DDAVP and DPP were carried out in CF-1 mice. RESULTS: DDAVP was readily reduced by a 2-fold molar excess of DTT at 37 degrees C for 0.5 hr. DPP was formed by the reaction of reduced DDAVP with Pal-CPD. Each DPP molecule contains two palmitic acid moieties, which link to the peptide via two disulfide bonds. After acid precipitation and size-exclusion chromatography, the purity was found to be approximately 95%, and the overall yield was 57%. When DPP was administered subcutaneously to Brattleboro rats, the potency of the anti-diuretic activity of DDAVP was enhanced to more than 250-fold. The plasma concentration of intravenously injected DDAVP in mice decreased rapidly during the first 20 min and followed by a slow elimination rate. However, in DPP administered mice, the plasma concentration actually increased in the first 20 min, followed by a slow elimination with a rate similar to that in DDAVP-injected mice. The regeneration of DDAVP was detected in the plasma of mice treated with DPP. Studies of the organ distribution in mice indicated that the liver retention of DPP was longer than that of DDAVP. On the other hand, the intestinal excretion of DPP was significantly less than that of DDAVP. CONCLUSIONS: The 250-fold increase of the anti-diuretic potency in DPP is most likely due to a slow elimination and prolonged tissue retention, together with the regeneration of active DDAVP, in the animals. Our results indicate that reversible lipidization is a simple and effective approach for improving the efficacy of many peptide drugs.

Animals↗
PubMed1999

Evidence for helicity in insect diuretic peptide hormones: computational analysis, spectroscopic studies, and biological assays.

The conformation of four insect diuretic hormones has been analyzed computationally using secondary structure prediction routines and comparison with structures in the Brookhaven Protein Databank. Based on this analysis, a common seven-residue peptide fragment (DVLRQRL) had a high probability of forming an alpha-helix. Circular dichroism (CD) studies found that addition of trifluoroethanol (TFE) to an aqueous solution of the seven-residue fragment induces a change from random coil to helix. Subsequent NMR studies in water-TFE (1:1) produced nOe values and 3JalphaNH coupling constants confirming a helical conformation: 3JalphaNH coupling constants for the first five residues (D1 to Q5) were all < or = 6.0 Hz and two medium-range nOe values (dalphaN (i,i+3)) were observed between V2 and Q5, and R4 and L7. The longer fragments PLDVLRQRL in water-TFE and Lom-DH 1-26 in water alone, both containing the DVLRQRL sequence of the locust (Locusta migratoria) diuretic hormone, maintained the helicity as determined by CD analysis. However, the remaining 20 residues of the locust diuretic hormone did not maintain the same amount of helicity in water and all of the truncated fragments were not biologically active.

Amino Acid Sequence↗
PubMed1981

Effects of diuretic and propranolol on plasma lipoprotein lipids.

Ticrynafen (TCNF), a nonthiazide diuretic, has been reported to be nonhyperlipidemic. To define the effects of these drugs on plasma lipoproteins, experiments were performed in hypertensive subjects after placebo therapy, 4 wk after therapy with either hydrochlorothiazide (HCTZ) or TCNF, 3 mo after diuretic with propranolol, and 1 mo after therapy with propranolol alone. Plasma lipoproteins were separated by ultracentrifugation and the lipid fractions isolated by extraction and silicic acid thin-layer chromatography. Plasma low-density lipoprotein (LDL) total cholesterol fell and high-density lipoprotein (HDL) total cholesterol rose in subjects receiving TCNF. TCNF had no effect on plasma low-density lipoprotein (VLDL) triglyceride or phospholipid. There was no significant changes in LDL or HDL total cholesterol in subjects on HCTZ. HCTZ tended to increase plasma VLDL triglyceride and phospholipid. The addition of propranolol to either diuretic had no effect on LDL or HDL total cholesterol but increased VLDL triglyceride, especially in subjects on HCTZ. Propranolol alone had no effect on any of the lipids measured.

Adult↗
PubMed1988

Increased nonrenal clearance and increased diuretic efficiency of furosemide in cystic fibrosis.

The pharmacokinetics of furosemide and its diuretic effect were studied in six patients with cystic fibrosis (CF) and in six age-matched healthy volunteers. Furosemide was given intravenously at a dose of approximately 0.5 mg/kg. Renal excretion of furosemide was decreased in CF because nonrenal clearance was more than twice as high as in controls (p = 0.03). Nonrenal clearance correlated with the volume of distribution (r2 = 0.52, p = 0.01), which makes a difference in the distribution and binding determinants for clearance. Another reason for increased nonrenal clearance could be induction of drug metabolism in CF, but the excretion of furosemide conjugate did not differ significantly between the groups. Although 26% less furosemide was excreted in CF than in controls (p = 0.03), the diuretic response (calculated as excretion of water and electrolytes) did not differ. Thus the diuretic efficiency was higher in CF for Na+ (p = 0.02), Cl- (p = 0.01), K+ (p = 0.07), and volume (p = 0.005). This difference is probably secondary to the different rates of delivery of furosemide into urine.

Adolescent↗