Drugs online research references
cornell.edu
Acute sodium depletion by furosemide induces a robust salt appetite in the rat which is satiated rapidly by ingestion of sodium chloride (salt) solutions. To identify neuronal populations activated by sodium depletion and by salt intake, we quantified c-fos-like immunoreactivity (c-FLI) in the subfornical organ (SFO) and nucleus of the solitary tract (NTS) after sodium depletion and at time intervals from 30 min to 12 h after 1 h of access to 0.3 M NaCl. Rats drank 10+/-1.6 mL over 1 h, with most of the intake occurring by 30 min. Increased numbers of c-FLI-positive cells were observed in the SFO 24 h after sodium depletion; c-FLI remained elevated for 90 min after 0.3 M NaCl intake and then declined until the number of c-FLI-positive cells at 12 h was not significantly different from mock-depleted levels. Sodium depletion alone did not significantly elevate c-FLI in the NTS, but the number of c-FLI-positive nuclei in the NTS was significantly increased after 0.3 M NaCl intake. The cellular location and temporal pattern of c-FLI expression are consistent with activation of neural circuitry sensitive to humoral, gustatory, and postingestive stimuli accompanying sodium depletion and 0.3 M NaCl ingestion. c-FLI in the SFO and NTS may serve as quantifiable markers in the central nervous system of the state of sodium depletion and of ingestive (orosensory and gastrointestinal) sensory stimulation, respectively.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9523891&dopt=Abstract
Biochem J. 1998 Sep 15;334 ( Pt 3):525-30.
Increased choline transport in erythrocytes from mice infected with the malaria parasite Plasmodium vinckei vinckei.
Staines HM, Kirk K.
Division of Biochemistry and Molecular Biology, Faculty of Science, Australian National University, Canberra ACT 0200, Australia.
Parasitized erythrocytes from mice infected with the murine malaria parasite Plasmodium vinckei vinckei showed a marked increase in the rate of influx of choline compared with erythrocytes from uninfected mice. In contrast, uninfected erythrocytes from P. vinckei-infected animals transported choline at the same rate as those from uninfected mice. The increased influx of choline into parasitized cells was via two discrete routes. One was a saturable pathway with a Km similar to that of the choline carrier of normal erythrocytes but a Vmax approx. 20-fold higher than that observed in uninfected cells. The other was a non-saturable pathway inhibited by furosemide. At choline concentrations within the normal physiological plasma concentration range, the former pathway contributed approx. two-thirds and the latter approx. one-third of the influx of choline into parasitized cells. The characteristics of the furosemide-sensitive pathway were similar to those of a broad-specificity pathway that is induced in human erythrocytes infected in vitro with Plasmodium falciparum. The results of this study rule out the possibility that the induced transport pathway of P. falciparum-infected erythrocytes is an artifact arising in vitro from the long-term culture of parasitized cells and provide evidence that this pathway makes a significant contribution to the uptake of choline into the parasitized cells of malaria-infected animals.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9729457&dopt=Abstract
Pflugers Arch. 1976 Sep 3;365(1):81-7.
Renal effects of furosemide in glycerol induced acute renal failure of the rat.
Greven J, Klein H.
The renal effects of furosemide in acute renal failure of the rat were studied using clearance and micropuncture techniques. Acute renal failure was induced by an intramuscular injection of 50% glycerol (10 ml/kg). Functional impairement of the glycerol treated animals consisted of a decrease in urinary sodium excretion, renal blood flow, total kidney GFR and effective filtration pressure of superficial nephrons. Effective filtration pressure was calculated from proximal free flow and stop flow pressure measurements. In contrast to control animals furosemide did not increase urine volume during acute renal failure due to a marked fall in GFR. Renal blood flow, as measured by an electromagnetic flowmeter, also decreased after furosemide in glycerol treated rats and increased in control animals. Furosemide reduced effective filtration pressure during acute renal failure to almost zero, whereas in control animals effective filtration pressure virtually remained constant.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=988544&dopt=Abstract
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