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PubMed1982

Hgcl2-induced acute renal failure in the rat. Effect of water diuresis, saline loading, and diuretic drugs.

A variety of pretreatment-treatment protocols were applied to rats with ARF induced by the subcutaneous injection of 6 mg of HgCl2 per kilogram body weight. Renin depletion induced by DOCA-saline pretreatment was associated with protection against HgCl2-induced ARF only when the saline diuresis was maintained by drinking 1% NaCl after injury. Twenty-four dehydration followed by free access to tap water annihilated the protective effect of DOCA-saline pretreatment despite maintained depletion of renal renin. Continuous intravenous loading with saline and furosemide, although increasing renal renin levels, afforded as much protection as saline loading alone. Ethacrynic acid, which did not increase salt excretion in our rats, as well as water diuresis, failed to be protective. A loose correlation was found between he amount of histological damage to the convoluted parts of the proximal tubules and the degree of renal functional impairment. Thus protection against HgCl2-induced ARF was independent of the renal renin level but closely related to urinary NaCl excretion after the injury. Saline diuresis could act by relieving or preventing tubular obstruction.

Acute Kidney Injury↗
PubMed2003

The effects of the loop diuretics furosemide and torasemide on diuresis in dogs and cats.

Torasemide is a new loop diuretic that combines the effects of furosemide and spironolactone. There are no reports on the effects of torasemide in cats and dogs. This study compared the diuretic effects of furosemide and torasemide in cats and dogs. Cats with pressure overload cardiac hypertrophy were given oral placebo, torasemide 0.3 mg/kg, or furosemide 1 mg/kg or 3 mg/kg. Control and mitral regurgitation dogs were given oral placebo, torasemide 0.2 mg/kg, and furosemide 2 mg/kg for 7 days. Urine samples were obtained at baseline and 1, 2, 3, 4, 5, 6, 8, 12, and 24 hr after each drug dose. Urine volume and urine Na(+) and K(+) were measured. Both furosemide and torasemide increased urine volume 1 hr after administration. Furosemide caused a dose-dependent increase in urine volume that peaked at 2-3 hr in cats and dogs. The diuretic effect of furosemide disappeared 6 hr after administration, while that of torasemide peaked 2-4 hr after administration and persisted for 12 hr in cats and dogs. In MR dogs, torasemide for 7 days significantly decreased urine potassium excretion. Plasma aldosterone increased with torasemide, whereas there was no change with furosemide. In conclusion, about 1/10 concentration of torasemide was as potent as furosemide and had a longer diuretic effect in cats and dogs. These data suggest that torasemide is useful for treating congestive heart failure or edema in cats and dogs.

Animals↗
PubMed1982

[Pharmacological studies on azosemide [5-(4'-chloro-5'-sulfamoyl-2'-thenylamino)-phenyltetrazole], a new diuretic (1) Effects on diuresis, plasma renin activity and urinary prostaglandin E excretion in normal rats (author's transl)].

Effects of azosemide on diuresis, plasma renin activity (PRA), and urinary prostaglandin E (PGE) excretion in normal rats and rats pretreated with indomethacin were studied in comparison with those of furosemide. Azosemide at doses ranging from 10 to 40 mg/kg p.o. dose-dependently increased urinary volume and Na+, K+, and Cl- excretions. In this case, the increases in urinary volume and Na+, K+, and Cl- excretions with 40 mg/kg of this drug were 3.4 and 4.1, 2.9, and 5.8 times, respectively. Pretreatment with indomethacin (10 mg/kg X 3 p.o.), a PG synthesis inhibitor, inhibited the increasing effects of this drug on urinary volume and Na+ and Cl-excretions by 80 or approximately 90%. Moreover, the increasing effects of this drug on PRA and urinary PGE excretion were also inhibited remarkably to the same degree by pretreatment with indomethacin. These effects of azosemide were roughly similar to those of furosemide. From these results, the diuretic action of azosemide, like that of furosemide, may partly be mediated through the activation of the PG system in kidney.

Animals↗