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Results for “DIURESIS AND DIURETICS”

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PubMed1987

Enhanced metabolic vasodilation secondary to diuretic therapy in decompensated congestive heart failure secondary to coronary artery disease.

Since sodium and water retention have been implicated as major factors limiting maximal metabolic vasodilation in congestive heart failure (CHF), the effect of rigorous diuresis on maximal vasodilatory capacity was studied systematically in 9 subjects hospitalized with decompensated CHF. Peak reactive hyperemic blood flow, measured by strain-gauge plethysmography, was used as an index of maximal vasodilatory capacity. After 24 hours of diuresis and a 2.2-kg weight loss, maximal flow increased from 19.9 to 26.1 ml/min X 100 ml (p less than 0.05). Despite a further 1.4-kg weight loss between 24 and 48 hours, maximal blood flow increased no more (26.1 to 25.8 ml/min X 100 ml). Since blood pressure did not change significantly, minimal forearm resistance and maximal conductance showed similar improvements. It is unlikely that vasoconstrictor hormone changes could account for this effect since a marked decrease in plasma norepinephrine occurred in only 2 of 8 subjects and plasma renin activity decreased in only 1 subject. As a group there was no significant change in norepinephrine level, which remained substantially above normal (1,525 to 1,148 pg/ml), or in plasma renin activity (12.3 to 18.9 ng/ml/hour). Because the improvement in vasodilator capacity reached a plateau by 24 hours despite continued diuresis, and because peak reactive hyperemic blood flow was still 32% below normal, it is suggested that a second mechanism besides sodium and water retention is responsible for a significant portion of the impaired peripheral vasodilation in CHF.

Aged↗
PubMed1985

[Diuretics].

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Aldosterone↗
PubMed1999

Urinary thiamine excretion in the rat: effects of furosemide, other diuretics, and volume load.

Long-term furosemide therapy is associated with increased urinary loss of thiamine. To examine the mechanism of furosemide-induced urinary thiamine loss, we measured urinary excretion of thiamine in rats in response to increasing doses of furosemide, acetazolamide, chlorothiazide, amiloride, mannitol, and extracellular fluid (ECF) volume loading by saline infusion. All animals were in normal thiamine balance as reflected by a thiamine pyrophosphate effect (TPPE) of 2.25% +/- 0.60% (mean +/- SEM), and all had normal renal function. Urinary flow increased in response to diuretic administration in a dose-dependent manner, reaching (mean) peak urinary flow rates of 283 to 402 microL/min. Fractional excretion of sodium (FE(Na)) exhibited the same pattern, reaching peak values of 12.3% to 23.2%. Urinary thiamine excretion increased in proportion to the incremental doses of diuretic agents, reaching (mean) maximal values of 7.44 to 9.34 pmol/min, with no significant difference (P = .11) between the various diuretics tested nor in response to saline loading. None of the diuretics tested differed in the effect on thiamine excretion, which was clearly flow dependent and only partially related to fractional sodium excretion. Urinary flow rate, being the single significant predictor, explained 78% (R2 = 0.78) of the variability in thiamine excretion rates. These findings indicate that urinary thiamine loss is caused by a nonspecific, flow-dependent mechanism common to all of the diuretics tested.

Animals↗
PubMed1988

Renal action of a novel uricosuric diuretic, S-8666. I. Clearance and tubular microinjection studies in rats.

Clearance and tubular microinjection techniques were used to evaluate the effects of a novel uricosuric diuretic, S-8666, on renal function and tubular absorption of urate by the rat kidney. Tubular sites of diuretic action of S-8666 were determined indirectly using osmolar clearance techniques. The i.v. injection of S-8666 at a dose ranging from 0.3 to 3.0 mg caused a dose-dependent increase in urine flow and sodium excretion. Potassium excretion was increased significantly but the increase was not marked as compared with sodium excretion. Glomerular filtration rate was not changed by S-8666. The diuretic response reached a maximum within 5 min and was retained for 45 min with 1 mg of S-8666. The comparison with the effect of furosemide revealed that furosemide was 13 times more potent than S-8666. Both the free water reabsorption on hydropenia and free water clearance in hydrated animals decreased with administration of S-8666. The urinary excretion of urate increased significantly after the administration of S-8666. By contrast, furosemide did not increase urinary excretion of urate. Total urinary urate recovery after S-8666 administration was higher after the microinjection of [14C]urate into early proximal tubule sites. We conclude that S-8666 acts as a uricosuric diuretic agent with the major site of altered urate absorption being in the proximal convoluted tubule and the major site of diuretic action being in the cortical and medullary diluting segments.

Animals↗
PubMed1977

[On the pharmacology of Etozolin (author's transl)].

Ethyl (Z)-(3-methyl-4-oxo-5-piperidino-thiazolidin-2-ylidene)acetate (etozolin, Gö 687, Elkapin) is a diuretic with a new chemical structure. Animal experiments with etozolin showed low toxicity, potent diuretic and saluretic properties with a mild onset of action. A marked antihypertensive effect was found in long-term experiments in hypertensive rats. In investigations concerning general pharmacology etozolin showed no effects which stand against its use as a diuretic.

Animals↗