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Results for “DIURESIS AND DIURETICS”

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At least 523 records · Page 29Linked to original sources
PubMed1979

Atrial reflexes and renal function.

Distension of small balloons in the venous-atrial junctions results in an increase in heart rate, urinary flow and sodium excretion. Two types of atrial receptors are described: one type, histologically known, discharging into myelinated fibers, and a second type, discharging into nonmyelinated ("C") fibers. These responses are mediated by the myelinated fibers. Experiments have shown that simulation of receptors discharging into the large myelinated vagal fibers is responsible for a reflex increase in heart rate mediated only by sympathetic nerves and for an increase in urinary flow. The efferent pathway of the diuretic response is shown to be nervous and hormonal. Stimulation of atrial receptors causes (1) a reduction of activity in nerves to the kidney, causing an increase in both urinary volume and sodium excretion, and (2) the release of a blood-borne agent, possibly diuretic, that increases urinary volume but does not affect sodium excretion.

Afferent Pathways↗
PubMed1993

Protective effect of inhaled piretanide on the bronchial obstructive response to ultrasonically nebulized H2O. A dose-response study.

Inhaled furosemide prevents the obstructive response to several bronchoconstrictor stimuli in asthma. To verify whether this protective effect is also shared by other loop diuretics, we investigated the effect of inhaled piretanide on the bronchial obstructive response to ultrasonically nebulized distilled water (UNW) in ten patients with moderate, stable asthma. In a randomized, single-blind dose-response study, each subject performed an UNW test immediately after nebulization of different doses of piretanide between 12 and 48 mg or placebo. The effect of a single 40-mg dose of inhaled furosemide was also investigated in six subjects. Piretanide caused a significant, dose-dependent increase in UNW PD20 with respect to placebo, corresponding to 0.6 +/- 0.2 doubling doses (mean +/- SE) after 12 mg, 1.3 +/- 0.2 after 24 mg, and 2.0 +/- 0.2 after 48 mg, and had a remarkable diuretic effect; 40 mg of furosemide increased UNW PD20 by 2.3 +/- 0.3 doubling doses (p < 0.01), but showed only a modest diuretic activity. These data indicate that inhaled piretanide is as effective as furosemide in preventing UNW-induced asthma, and this effect is unrelated to their diuretic potency.

Adult↗
PubMed1979

The effects of ticrynafen in the rat.

The effects of ticrynafen, a uricosuric diuretic, were examined utilizing free-flow micropuncture and clearance techniques in the rat. The intravenous infusion of ticrynafen (50 mg/kg body wt/hr) had no effect on glomerular filtration rate, but resulted in significant increases in urine flow from 4.4 +/- 0.7 microliter/min/g kidney wt to 19.2 +/- 2.6 (p less than 0.001); in urinary sodium excretion from 0.14 +/- 0.07 micronEq/min/g kidney wt to 2.35 +/- 0.52 (p less than 0.01); and in urinary urate excretion from 2.8 +/- 0.2 microgram/min/g kidney wt to 4.0 +/- 0.2 (p less than 0.005). There was no change in urinary phosphate excretion. The end-proximal TF/Pinulin ratio was 2.66 +/- 0.18 in control and 2.67 +/- 0.16 in experimental periods (p=NS). In awake animals, ticrynafen administration resulted in a decrease in CH2O from 6.47 +/- 0.12% to 3.50 +/- 0.69 (p less than 0.05), but no change in TCH2O. These studies demonstrate that ticrynafen is a uricosuric and diuretic agent in the rat. The natriuresis appears to derive from an inhibitory action of this agent in the cortical diluting segment of the nephron. In comparison to a related uricosuric diuretic, MK-196, ticrynafen is a less potent agent with respect to both its uricosuric and diuretic properties in the rat.

Absorption↗
PubMed1978

Pharmacological analysis of the action of diuretics in the newborn pig.

The effects of furosemide, ethacrynic acid, hydrochlorothiazide and amiloride on renal function of newborn piglets, 5 to 10 days old, were evaluated. Furosemide and ethacrynic acid were the most effective diuretics. Furosemide infusion at 0.5 mg/kg/hr inhibited reabsorption of 21% filtered sodium and ethacrynic acid, 1 mg/kg/hr, increased fractional sodium excretion to 29%. Hydrochlorothiazide infusion produced a milder natriuresis than furosemide or ethacrynic acid. Infusion of hydrochlorothiazide at 1.0 mg/kg/hr increased fractional sodium excretion from 0.3% during the control period to 7.2%. Furosemide, ethacrynic acid and hydrochlorothiazide each increased potassium excretion to near 20 microEq/min. amiloride (1.0 mg/kg/hr) increased fractional sodium excretion from 0.2% during control period to 2.8% during drug infusion but did not affect potassium excretion. When infused in combination with furosemide and hydrochlorothiazide, amiloride increased the natriuresis and decreased the kaliuresis of both diuretics. It is concluded that the unanesthetized piglet is a good model for renal function of immature mammals and responds to diuretics in a manner qualitatively similar to adults.

Animals↗
PubMed1989

Additive diuretic effect of S-8666 during furosemide-induced diuresis in rats.

In order to verify that the novel uricosuric loop-acting diuretic S-8666 has an additional site of action in the distal tubule, we investigated the additive diuretic effect of S-8666 during furosemide-induced diuresis in rats. Intravenous bolus injection of S-8666 (3-30 mg/kg) and trichlormethiazide (TCM) (1-10 mg/kg) caused dose-dependent increases in Na+ excretion during furosemide-induced diuresis (primary, 10 mg/kg i.v.; sustaining, 10 mg/kg/hr i.v.), whereas injection of furosemide (5 mg/kg) did not. Ca++ excretion was decreased by injection of each drug. A significant reduction in Ca++/Na+ was observed at all doses of S-8666 and TCM. Additional natriuretic and hypocalciuric effects were lower in the S-8666 than in the TCM group. From these observations we conclude that: 1) S-8666 has a natriuretic effect which is additive to that of furosemide; 2) S-8666 attenuates the calciuric effect of furosemide; and, 3) S-8666 may have an additional site of action in the distal tubule.

Animals↗
PubMed1984

Role of the renal prostaglandins in furosemide-induced diuresis.

The role of the renal prostaglandin (PG) system in the renal effects of furosemide was assessed by using indomethacin, an inhibitor of PG synthetase, in conscious rats under conditions of vasopressin infusion (or dehydration). Urinary PGE and PGF2 alpha were measured by radioimmunoassay under conditions of furosemide-induced diuresis. The diuretic and natriuretic effects of furosemide were accompanied by a concomitant increase in the urinary excretion of PGE. In normal rats the pretreatment of indomethacin at 10 mg/kg failed to alter the diuretic effect of furosemide (5 mg/kg). In contrast, the diuretic effect of furosemide in vasopressin (2 U/kg)-infused (or dehydrated) rats was greatly inhibited by indomethacin. In regard to the natriuretic effect of furosemide, indomethacin did impair this response to furosemide both in normal and vasopressin-infused (or dehydrated) rats, but inhibited more strongly in the latter than in the former. These results suggest that the renal PGE is necessary for furosemide to produce optimal diuretic and natriuretic effects under conditions of vasopressin infusion (or dehydration).

Animals↗