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At least 1,783 records · Page 99Linked to original sources
PubMed1983

[Low renin variant of hypertension: functional relations of the renin-aldosterone pressor system].

Renin-aldosterone function was studied in 23 patients with low-renin essential hypertension (LREH) under resting and stimulated conditions. Patients were selected on the basis of differential diagnostic tests of renin-angiotensin stimulation and inhibition as well as roentgeno-radiologic findings in order to rule out adrenal lesions. The results were compared with those of patients with primary aldosteronism and with essential hypertension where renin activity can be stimulated under similar sodium balance conditions. Intravenous or prolonged furosemide administration was shown to be the test of choice for the diagnosis of renin suppression. The renin-aldosterone system of LREH patients featured subnormal renin activity and normal aldosterone levels in baseline conditions, and the lack of renin stimulation together with limited aldosterone stimulation following functional tests. The analysis of changes in diuresis, natriuresis and the pattern of Na/K coefficient points to a great diuretic and natriuretic effect of furosemide in patients with LREH.

Aldosterone↗
PubMed1982

Choleretic and diuretic properties of dihydroxydibutyl ether in the rat.

Dihydroxydibutyl ether (DDE) induces a choleresis and a diuresis in the rat. The stimulation of bile flow is immediate and dose-dependent; DDE appears to stimulate bile acid-independent flow of canalicular origin, because erythritol clearance increased in parallel to bile flow and choleresis occurs in the absence of an increased bile acid secretion. Increased bile flow may be accounted for by the osmotic activity of DDE and DDE metabolites excreted into bile, with an average increase in bile flow of 16 microliters/mumol of DDE (or DDE metabolites). Biliary secretion of DDE is limited with a maximal rate (biliary Tm) of 773 nmol.min-1.100 g b.wt.-1. The metabolic products of DDE in bile appear to be its mono- and diglucuronide conjugates inasmuch as DDE can be recovered after beta-glucuronidase incubation. DDE and a DDE glucuronide conjugate are also detected in the urine: there is an apparently linear relation between DDE (and DDE metabolites) excretion rate and increase in urinary flow (3.5 microliters/mumol of DDE or DDE metabolites). It is concluded that DDE stimulates choleresis and diuresis in the rat because the molecule and its glucuronide conjugates are secreted and concentrated in bile and urine.

Animals↗
PubMed1988

Pressure-diuresis in volume-expanded rats. Cortical and medullary hemodynamics.

This study evaluated whether pressure-diuretic and pressure-natriuretic responses are associated with alterations in vasa recta hemodynamics. Autoregulation of cortical and papillary blood flow was studied using a laser-Doppler flowmeter in volume-expanded and hydropenic rats. Superficial cortical flow and whole kidney renal blood flow were autoregulated in volume-expanded rats and decreased by less than 10% after renal perfusion pressure was lowered from 150 to 100 mm Hg. In contrast, papillary blood flow was not autoregulated and fell by 24 +/- 2%. The failure of papillary blood flow to autoregulate was due to changes in the number of perfused vessels as well as to alterations in blood flow in individual ascending and descending vasa recta. Pressure in vasa recta capillaries increased from 6.8 +/- 0.8 to 13.8 +/- 1.2 mm Hg after renal perfusion pressure was elevated from 100 to 150 mm Hg, and renal interstitial pressure rose from 7.4 +/- 0.8 to 12.3 +/- 1.4 mm Hg. In hydropenic rats, papillary blood flow was autoregulated to a significant extent, but it still decreased by 19% after renal perfusion pressure was lowered from 150 to 100 mm Hg. The pressure-diuretic and pressure-natriuretic responses in hydropenic rats were blunted in comparison to those observed in volume-expanded rats. These findings indicate that the pressure-diuretic and pressure-natriuretic responses are associated with changes in vasa recta hemodynamics and renal interstitial pressure.

Animals↗
PubMed1992

The importance of renal function in the interpretation of diuresis renography.

Interpretation of the diuresis renogram is dependent on a full understanding of the factors that contribute to the washout curve, a major determinant being the urinary flow rate induced by the diuretic. Frusemide-induced flow rates were measured in 86 patients over a 30-min period and related to creatinine clearance in 39, 99mTc-DTPA clearance (glomerular filtration rate (GFR)) in 27, and 123I-Hippuran clearance (effective renal plasma flow) in 20. The flow rates 3 to 6 min and 15 to 18 min after administration of the diuretic received specific attention because of their importance to F + 20 and F - 15 diuresis renography respectively. The mean urinary flow rate 15 to 18 min after frusemide was 3.5 ml/min greater than at 3 to 6 min (P less than 0.001), explaining the value of the F - 15 renogram in further evaluating equivocal F + 20 curves. Linear relationships were observed between each parameter of function and the 3 to 6 min and 15 to 18 min periods as follows: creatinine clearance r = 0.66, r = 0.77; 99mTc-DTPA clearance r = 0.66, r = 0.77; 123I-Hippuran clearance r = 0.59, r = 0.71. From regression analysis of the data presented it is possible, with knowledge of total and split function, to predict single-kidney flow rates. It is demonstrated that these may commonly exceed flow rates used for perfusion studies if function is normal, but a single-kidney flow rate of 10 ml/min is unlikely to be attained if the single-kidney GFR is less than 15 ml/min.

Adult↗
PubMed1994

Contribution of alpha-2 adrenoceptors to kappa opioid agonist-induced water diuresis in the rat.

Clearance studies in rats using kappa opioid agonists have demonstrated that agonists that can cross the blood-brain barrier are more potent water diuretics than agonists which have limited access to the brain. The mechanism of kappa agonist-induced water diuresis is unclear but may involve inhibition of vasopressin secretion and/or an adrenomedullary factor. In the present study the effect of an alpha-2 adrenoceptor antagonist (yohimbine, 10 micrograms/kg.min i.v.) on kappa agonist-induced water diuresis was evaluated in conscious chronically instrumented rats. BRL 53117 (1-[(3,4-dichlorophenyl)acetyl]-2-[(3-hydroxy-1-pyrrolidinyl) methyl]4,4-dimethyl piperidine), a kappa agonist that can cross the blood-brain barrier, caused a dose-dependent (1-100 micrograms/kg) water diuresis which was attenuated by yohimbine. The effective dose to cause a free water clearnace of zero for BRL 53117 was 13 +/- 5 micrograms/kg in vehicle-treated rats and 37 +/- 12 micrograms/kg in yohimbine-treated rats. BRL 52974 (5-[(3,4-dichlorophenyl)acetyl]4-(1-pyrrolidinylmethyl)-4,5,6,7-te trahydro- 1H-imidazo[4,5-c]pyridine), a compound with limited ability to cross the blood-brain barrier, also caused a dose-dependent water diuresis, albeit at higher doses (30-3000 micrograms/kg), and thus a higher effective dose to cause a free water clearance of zero (129 +/- 61 micrograms/kg); however, the effect was abolished by yohimbine. The data suggest that kappa agonists cause a water diuresis by both a central mechanism involving inhibition of vasopressin secretion and a peripheral mechanism involving stimulation of renal alpha-2 receptors.

Animals↗
PubMed1992

Diuresis increases ascitic fluid opsonic activity in patients who survive spontaneous bacterial peritonitis.

Patients with low protein ascites and deficient ascitic fluid opsonic activity have been shown to be unusually predisposed to development of spontaneous bacterial peritonitis. Survivors of spontaneous peritonitis frequently develop recurrent infection. Diuresis has been shown to increase the ascitic fluid opsonic activity of patients who have never had spontaneous bacterial peritonitis. Patients with adequate opsonic activity are protected from ascitic fluid infection. Theoretically, the subset of patients who develop spontaneous peritonitis may have such severe liver disease that (i) their ascites is refractory to diuretic therapy or (ii) their ascitic fluid opsonic activity does not increase in response to diuresis. In this study, opsonic activity and concentrations of total protein and complement components were measured in the ascitic fluid of 11 patients who were hospitalized with spontaneous bacterial peritonitis and who responded to oral diuretics. The mean values of all of these parameters were found to increase significantly comparing the end-of-diuresis samples to the specimens that were diagnostic of ascitic fluid infection. Patients who survive spontaneous bacterial peritonitis are able to increase their ascitic fluid total protein and opsonic activity in response to diuresis. This increase in endogenous antimicrobial activity may help prevent recurrence of ascitic fluid infection.

Amiloride↗
PubMed1996

Effect of furosemide oral solution versus furosemide tablets on diuresis and electrolytes in patients with moderate congestive heart failure.

Oral furosemide solution was claimed to produce a greater diuretic response than furosemide tablets in patients with congestive heart failure. The aim of this study was to assess this observation and to further investigate the effects on the electrolyte balance. We compared the effects of oral furosemide in tablets versus oral furosemide solution on serum levels as well as on 4- and cumulative 24-hour urinary volume and sodium, potassium, calcium, magnesium and zinc excretions in 10 patients with moderate congestive heart failure due to ischemic heart disease. Oral furosemide (40-80 mg) was given at the usual once-daily dosage. No change in serum electrolyte levels has been found. All urinary parameters, except zinc, were significantly greater during the first 4 h following oral solution as compared with tablets (volume p < 0.001, sodium p < 0.001, potassium p < 0.05, calcium p < 0.003, magnesium p < 0.05). However, after 24 h, significant differences were found in urinary volume (p < 0.03) and sodium excretion (p < 0.004) only. We conclude that: (1) oral furosemide solution provides a more potent 24-hour diuretic and natriuretic effect than an identical dosage in tablet form, without entailing greater cumulative urinary losses of potassium, calcium, magnesium, and zinc; (2) following the first 4 h of furosemide solution, brisk diuresis, kaliuresis, and magnesiuria are produced, and (3) despite the urinary losses, serum electrolytes remained within normal limits at 4 and 24 h.

Aged↗
PubMed1996

[Diuretics in renal failure].

The indications for the use of diuretics in patients with renal failure are edema and hypertension. An ancillary measure is dietary sodium restriction which permits reduction of the diuretic dose and reduces the frequency of diuretic induced side effects. The natriuretic action of diuretics is attenuated in renal failure both for pharmacokinetic and pharmacodynamic reasons. The most important cause for reduced efficacy of diuretics in renal patients is binding of diuretics to proteins within the tubular lumen so that the absolute free concentration of diuretics is diminished. Further important reasons for the diminished increment in urinary sodium excretion that is seen in patients with renal failure include a) reduced number of nephrons (i.e. reduced functional mass) and b) intrarenal compensatory mechanisms which increase sodium activity and tubular reabsorption of sodium. These difficulties can be overcome by dietary sodium restriction, by selection of higher doses of diuretics, by selection of appropriate intervals of administration and by combination of loop diuretics and thiasides. In order to recognize side effects resulting from excessive diuresis with hypovolemia and increase of serum creatinine concentration from prerenal causes it is necessary to closely monitor the patients.

Antihypertensive Agents↗
PubMed1976

Clonidine-induced increase of renal prostaglandin activity and water diuresis in conscious dogs.

I.v. administration of clonidine to conscious dogs induces a water diuresis with hyposmotic urine and minor effect on electrolyte excretion. The diuresis is preceded by an increased urinary PGE excretion, but no change of urinary ADH output is observed. Plasma renin activity decreases. Both ADH infusion and indomethacin pretreatment inhibit the diuretic effect of clonidine. The results support the hypothesis that clonidine-induced water diuresis is mediated via an anti ADH effect due to increased renal prostaglandin activity. Moreover the results suggest that there is no direct stimulation of renin release by PGE.

Animals↗
PubMed1989

Effects of diabetes and diuresis on contraction and relaxation mechanisms in rat urinary bladder.

Experiments were designed to gain information on the mechanisms leading to diabetic urinary bladder dysfunction. Bladders from control rats, animals subjected to 4-5 wk streptozocin-induced diabetes, and rats subjected to equivalent diuresis produced by 5% sucrose feeding were studied with an in vitro whole-bladder preparation and neurochemical measurements. The diuretic group was used to distinguish alterations produced by metabolic effects on nerve and muscle from those induced by prolonged periods of excessive diuresis. Diuresis alone explains many of the diabetes-induced effects, including decreased norepinephrine levels, postsynaptic supersensitivity for sympathetic regulation of bladder storage, decreased responsiveness to parasympathetic regulation of emptying, and enhanced prostaglandin F2 alpha-induced contraction. Other diabetes-induced effects were not observed in the diuretic controls and are presumed to result from metabolic alterations associated with diabetes. These effects were decreases in norepinephrine uptake and in choline acetyltransferase activity, both markers of nerve terminal function. Thus, diuretic and metabolic factors appear to contribute to the early signs of parasympathetic and sympathetic neuropathy. In contrast, we found no evidence for loss of sensory nerve function in the diabetic bladder, at least at the organ level, because no diabetes- or diuresis-induced changes were observed in responsiveness to substance P or capsaicin.

Aminophylline↗
PubMed1996

Benefits and risks of torasemide in congestive heart failure and essential hypertension.

Torasemide is a lipophilic anilinopyridine sulphonylurea derivative that acts as a high ceiling loop diuretic and has been used for the treatment of both acute and chronic congestive heart failure (CHF) and hypertension. Torasemide is similar to other loop diuretics in terms of its mechanism of diuretic action; namely, blockade of Na+/K+/2Cl- cotransport in the thick ascending limb of the loop of Henle. It has high bioavailability (> 80%), as does bumetanide, but a longer elimination half-life (3 to 4 hours) than either bumetanide or furosemide (frusemide). In the treatment of chronic CHF, oral torasemide (5 to 20 mg/day) has been shown to be an effective diuretic. Patients treated with torasemide for up to 1 year have reduced bodyweight, improved pulmonary haemodynamics, and decreased CHF severity. Intravenous torasemide (20 to 60mg as a single dose) has been shown to be as effective as furosemide in the treatment of acute CHF, and resulted in significant diuresis, bodyweight loss, and improved pulmonary haemodynamics and exercise performance. 'Non-diuretic' dosages (2.5 to 5 mg/day) of oral torasemide have been used to treat essential hypertension, both as monotherapy and in combination with other antihypertensive agents. When used in these dosages, torasemide lowered diastolic blood pressure (DBP) to below 90mm Hg in 8 to 12 weeks in 70 to 80% of patients. With dose doubling, this level of efficacy occurred in more than 90% of hypertensive patients. Clinical trials have established that blood pressure can be maintained at this level for at least 1 year with low dose torasemide. Torasemide is well tolerated in dosages up to 20 mg/day for at least 1 year. The most commonly reported adverse effects are those associated with loop diuretics in general. These include transient hypokalaemia, hyperuricaemia, dizziness, headache, gastrointestinal disturbances, orthostatic hypotension and fatigue. Adverse effects are comparable with those of other diuretics and rarely necessitate drug withdrawal.

Antihypertensive Agents↗