Drugs online research references
Acta Physiol Scand. 1988 Jan;132(1):75-81.
Furosemide causes acute and long-term hyperglycaemia and reduces glucose tolerance in mice.
Sandstrom PE, Sehlin J.
Department of Histology and Cell Biology, University of Umea, Sweden.
The effect of furosemide on carbohydrate metabolism was studied in mice. Single-dose administration (200 mg kg-1 body weight) resulted in transient hyperglycaemia and a rise in the glucose/insulin ratio within 60 min. The glucose tolerance was impaired with elevated serum glucose and reduced insulin response 2 h after the furosemide injection, but had recovered within 24 h. In mice made hypoglycaemic by prior injection of insulin, the basal serum glucose and the glucose tolerance were impaired 22 h after the injection of furosemide. It is suggested that furosemide has both acute and long-term effects on carbohydrate metabolism in mice and that, at least in part, this is due to reduced insulin secretion. Glucose may protect against the diabetogenic action of furosemide.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3066121&dopt=Abstract
Am J Physiol. 1988 Sep;255(3 Pt 1):G367-73.
Cl(-)-HCO3- antiport in rat lacrimal gland.
Lambert RW, Bradley ME, Mircheff AK.
Department of Physiology and Biophysics, University of Southern California School of Medicine, Los Angeles 90033.
With the use of analytical subcellular fractionation and tracer uptake methods we have demonstrated the presence of a Cl(-)-HCO3- antiport mechanism in the rat exorbital lacrimal gland. We find that outwardly directed gradients of HCO3- and of 35Cl- accelerated the flux of 36Cl- into isolated membrane vesicles. Because vesicle membrane potentials were clamped to 0 mV with K+-valinomycin, the observed anion gradient-dependent acceleration of Cl- influx could not be attributed to conductive fluxes. The antiporter had an apparent K0.5 for Cl- between 6 and 10 mM. It was sensitive to the stilbene derivatives 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). It was also sensitive to the loop diuretic furosemide, which has frequently been used in tests for NaKCl2 symporter activity. Other anions inhibited anion gradient-driven Cl- influx in the sequence SCN- greater than NO3- greater than Cl- greater than HCO3- greater than SO2-4. The density distribution of Cl(-)-HCO3- antiport activity indicated that approximately 80% of the transporter was associated with intracellular membranes, suggesting the presence of cytoplasmic pools of functional antiporters. Because several studies have already shown the presence of Na+-H+ antiporter activity in lacrimal acinar cell basolateral membranes, a cellular model for lacrimal acinar electrolyte secretion is proposed in which a parallel array of Cl- -HCO3- and Na+-H+ antiporters mediates the Na+-dependent accumulation of Cl- against its electrochemical potential gradient.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3421339&dopt=Abstract
J Surg Res. 1985 Mar;38(3):216-23.
Furosemide during sustained left atrial hypertension in functionally anephric dogs: intravascular and extravascular pulmonary fluid volumes. V.
Slutsky RA, Olson LK, Dittrich HC.
The response of intravascular (PBV) and extravascular (EVLW) pulmonary fluid volume was examined using double-indicator techniques (thermal-green dye) in 11 open-chest anesthetized dogs during the production of sustained left atrial (LA) hypertension by a LA balloon over a period of 195 min. In 6 of these animals data were also acquired after the intravenous administration of furosemide (1 mg/kg). The renal effects of the diuretic were blocked by tying off the ureters and the vascular supply of both kidneys. Left atrial pressure (N = 11) was abruptly increased from 2.2 +/- 2.1 mm Hg to 30.2 +/- 4.0 mm Hg (P less than 0.01) and maintained at that level for 120 min. Data were obtained prior to pressure elevation, immediately upon pressure elevation, and then every 60 min for a total of 120 min. At that point EVLW had increased (8.1 +/- 0.8 cc/kg at control to 21.7 +/- 2.0 cc/kg at 120 min, P less than 0.001), as had PBV (6.2 +/- 2.1 cc/kg to 9.1 +/- 3.1 cc/kg P less than 0.01). After furosemide injection (N = 6), LA pressure declined (mean peak reduction of approximately 6 mm Hg at 60-75 min, P less than 0.01), aortic and pulmonary arterial pressure both declined (P less than 0.01). However, EVLW remained unchanged, though PBV decreased significantly (peak decrease at 75 min after furosemide administration of 2.0 +/- 0.4 cc/kg, P less than 0.01). In the untreated dogs, EVLW continued to climb (P less than 0.05 vs treated dogs at 75 min postfurosemide).(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3884897&dopt=Abstract
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