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At least 19 recordsLinked to original sources
PubMed1997

Inhibition of angiotensin-converting enzyme modulates structural and functional adaptation to loop diuretic-induced diuresis.

The roles of elevated cell sodium concentrations and the angiotensin-aldosterone system (AAS) in the structural and functional adaptation of the distal tubule and collecting duct system to a chronic increase of sodium delivery were examined using electron microprobe and quantitative morphologic/stereologic analyses. Studies were performed on rats given the loop diuretic torasemide acutely (20 min) or chronically (12 days), either alone or in combination with the angiotensin-converting enzyme (ACE) inhibitor, enalapril. In the sodium-absorbing cells of the distal tubule and cortical collecting duct-that is, in distal convoluted tubule (DCT), connecting tubule (CNT) and principal cells-an acute increase in sodium delivery caused a significant rise in intracellular sodium concentration and rubidium uptake, the latter an index of in vivo Na,K(Rb)-ATPase activity. The elevated cell sodium concentrations returned to, or close to, control values during chronic torasemide treatment. Intracellular rubidium concentrations, measured after a 30-second rubidium exposure, were not different from controls in DCT and CNT cells but were still higher in principal cells. Since, however, the distribution space for rubidium was significantly increased in chronic torasemide animals, rubidium uptake, and hence Na,K-ATPase activity, must have increased in proportion to cell volume in DCT and CNT cells, but more than proportionately in principal cells. When ACE was inhibited during chronic torasemide, the epithelial volume of DCT and cortical collecting duct (CCD) was increased mainly by lengthening and not, as was the case in rats given torasemide alone, by thickening of the tubule wall. Adaptation of the proximal tubule exclusively by lengthening was not affected by inhibition of the ACE. These data indicate that changes in cell ion composition may participate in initiating cell processes leading to adaptation of distal nephron segments to chronically increased salt delivery. Inhibition of the ACE reverses the torasemide-induced increase in apparent Na pump density in principal cells and seems to shift the relationship between hypertrophy and hyperplasia noted in DCT and CCD after chronic torasemide in favor of hyperplasia.

Aldosterone↗
PubMed1977

Acute acetylsalicylic acid poisoning: treatment with forced alkaline diuresis and diuretics.

101 patients were treated for acute acetylsalicylic acid (ASA) poisoning in the Nephrological Unit Trondheim between 1971-1975. On admission 33 of them had a serum salicylic acid (SA) concentration greater than 400 microgram/ml (mean 588 +/- 40 microgram/ml). This group was compared with a group of 11 children less than 5 years old with ASA poisoning and a mean serum SA on admission of 550 +/- 34 microgram/ml. Blood pH on admission was normal or elevated in all patients more than 12 years old (mean 7.43 +/- 0.01), whereas 7 of the 11 children suffered from metabolic acidosis. The results of forced alkaline diuresis produced by loop diuretics (bumetanide, furosemide) in ASA poisoned patients older than 12 years are reported. The mean T 1/2 of SA was 9.6 h in the treated group as compared to 18-22 h in untreated patients. There was no apparent difference between the diuretic effect of bumetanide and furosemide.

Acid-Base Equilibrium↗
PubMed1984

The effects of two combinations of a beta-blocker and a diuretic on diuresis in normal subjects.

Combinations of a beta-blocker and a diuretic often produce a greater fall in blood pressure than does either drug alone. Furthermore, beta-blockers prevent an increase in plasma renin activity, thereby attenuating diuretic-induced potassium excretion and also the reduction in hypotensive response to the diuretic. This study was designed to compare the effects of the two fixed-dose combinations atenolol 100 mg plus chlorthalidone 25 mg (Tenoretic; ICI) and sotalol 320 mg plus hydrochlorothiazide 50 mg (Sotazide; B-M) on the pattern of diuresis and the biochemical composition of the urine in normal subjects. These preparations differ mainly in that the plasma half-lives of chlorthalidone and hydrochlorothiazide are 60 hours and 6 hours respectively; the former therefore accumulates when given once daily while the latter does not. These two preparations were found to have similar effects on the pattern of diuresis and the biochemical values. It is therefore concluded that the relationship between the serum chlorthalidone level and the fall in serum potassium level is in keeping with the flat dose-response curves for the thiazide and phthalimide diuretics.

Adult↗
PubMed1975

Changes in urea clearance after a single dose of diuretics during water diuresis.

The action of various diuretics on the excretion fraction of urea (Curea/Ccr) was studied in 91 healthy volunteers under conditions of maintained maximal water diuresis. On the basis of previous data on transtubular transport or urea it should be expected that with an increase in the excretion fraction of water (V/Ccr) under the given experimental conditions we should find an increase in Curea/Ccr. After administration of polythiazide, which has a predominantly distal localisation of action in the nephron, Curea/Ccr did not change. After administration of chlorothiazide, furosemide and after i.v. administration of ethacrynic acid there was a marked increase in V/Ccr, ranging from 5.4 to 18%. Despite this there was no significant increase in Curea/Ccr. After i.v. administration of acetazolamide or oral administration of ethacrynic acid Curea/Ccr even showed a statistically significant decrease. These findings suggest that a decrease in proximal tubular reabsorption of water after administration of diuretics during maximal water diuresis is not a decisive factor for the renal excretion of urea. The data suggest that the diuretics affected the permeability of the distal segment of the nephron for urea in the sense of an increase of tubular reabsorption.

Acetazolamide↗
PubMed1986

Selected mechanisms of diuretic-induced electrolyte changes.

Thiazide diuretic therapy has been associated with several biochemical electrolyte imbalances including potassium loss. The onset, duration and magnitude of potassium excretion can influence decisions concerning drug therapy, particularly in hypertensive patients at risk if they develop diuretic-induced hypokalemia. The potassium depletion seen during the course of antihypertensive therapy with thiazides is brought about by 2 primary mechanisms: the increased delivery of sodium to the distal tubules for sodium-potassium exchange, and the development of secondary hyperaldosteronism, which causes resorption of sodium with a loss of potassium into the urine. The diuresis caused by thiazides is maximal between 8 and 12 hours. However, resultant volume contraction stimulates elevated serum aldosterone levels, which can be present for 24 hours or longer. Therefore, potassium loss may exceed the period of diuresis. Diuretics are effective antihypertensive therapy in many patients with mild hypertension. Potassium-sparing agents can offset potassium imbalance that often occurs with diuretics, and thus, these agents have become an important addition to the physician's treatment armamentarium for appropriate patients.

Aldosterone↗