Drugs online research references
Prostaglandins. 1978 Feb;15(2):255-66.
Prostaglandin (PG) analysis in urine of humans and rats by different radioimmunoassays: effect on PG-excretion by PG-synthetase inhibitors, laparotomy and furosemide.
Scherer B, Schnermann J, Sofroniev M, Weber PC.
The radioimmunological (RIA) determination of prostaglandin (PG) E2 and of PGF2alpha in urine of humans and rats is described in detail. After extraction and chromatography PGE2 was determined by using a PGE specific antibody or by using either PGB or PGF2alpha specific antibodies after the respective conversion procedures. The three different RIA procedures were compared to each other. PGF2alpha was determined by a specific antibody to PGF2alpha. Basal excretion of PGE2 and of PGF2alpha in healthy women on free diet was 9.3 ng/hour+/-0.98 and 18.3 ng/hour +/- 2.5 respectively. Furosemide increased the excretion of PGE2 and of PGF2alpha in humans significantly, while PG-excretion rates decreased on indomethacin. In rat urine PGE2 and PGF2alpha increased markedly from 46.2 pg/min +/- 9.3 and 27+/- 3.4 to 253.8 +/- 43.3 and 108 +/- 12.6 pg/min (per one kidney) in the anesthetized-laparotomized animal. This increase was abolished after giving two different PG synthetase inhibitors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=416466&dopt=Abstract
J Membr Biol. 1983;75(3):205-18.
Influx mechanisms for Na+ and Cl- across the brush border membrane of leaky epithelia: a model and microelectrode study.
Baerentsen H, Giraldez F, Zeuthen T.
This paper presents a numerical model for the movement of Na+, K+, Cl-, H+ and HCO3- in a leaky epithelium. The model describes the active transport of Na+ and K+ at the serosal membrane and electrodiffusive permeation across the mucosal, serosal and junctional pathways. The model accounts for H+ and HCO3- production in the cell. The influx of Na+ and Cl- is assumed to occur mainly via Na/H and Cl/HCO3 exchange. The behavior of the cell, with this influx mechanism, is compared to a cell with an obligatory neutral coupled influx of Na+ and Cl-. All parameters are obtained from the literature, primarily from studies utilizing the Necturus gallbladder. The analysis shows (i) that it is virtually impossible in steady-state experiments to distinguish between cells with Na/H - HCO3/Cl transport and cells with Na/Cl transport mechanisms. (ii) That nonsteady-state experiments can decide whether Na/H - HCO3/Cl or Na/Cl transport mechanisms mediate the influx of salt. A comparison between studies with ion-selective microelectrodes and the model predictions indicates that the influx of Na+ and Cl- is mediated by Na/H - HCO3/Cl transport when the external solutions contain CO2 and HCO3. (iii) The model also explains the diuretic effects of furosemide and carbonic anhydrase inhibitor, as well as the stimulatory effects on salt transport of elevated levels of HCO3- at a constant pH. (iv) The model fails to explain some experiments performed in HCO3/Co2-free media and some experiments using inhibitors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6313929&dopt=Abstract
Cell. 1979 Sep;18(1):153-63.
Increased sodium ion influx is necessary to initiate rat hepatocyte proliferation.
Koch KS, Leffert HL.
Serum-free media containing 10-50 ng insulin, glucagon and epidermal growth factor (EGF) ml-1 stimulate adult rat hepatocyte proliferation in 10-15 day old primary liver cell cultures. The kinetics of this response simulate hepatocellular transitions that accompnay liver regeneration after 67% hepatectomy. Amiloride, a Na+ influx inhibitor, reversibly blocks these transitions in vitro (ID50 approximately 0.02 mM) and in vivo (ID50 approximately 25 mg kg-1). Inhibition is observed with other cation flux modulators, including ouabain (ID50 approximately 0.2 mM), 0.2 microM monensin and 0.2 microM nigericin, but not with 0.3 mM furosemide or tetrodotoxin. The prereplicative interval in culture (0-12 hr) is characterized by preferential cellular responsiveness to EGF (0-3 hr) followed by insulin plus glucagon (3-12 hr). Parallel culture and animal studies show that the amiloride-sensitive and prereplicative intervals coincide. In culture, a "burst" of 22Na+ influx, stimulated by peptide-supplemented media within 1 min but decreased later at 12 hr, is retarded by amiloride. This drug also blocks delayed prereplicative events involving increased amino acid "A" transport system function at 4-8 hr, and 3H-uridine and 3H-leucine incorporation into RNA and protein, respectively, at 8-12 hr. These findings suggest that at least two time-ordered processes are necessary to initiate hepatic growth fully: first, activation of Na+ flux systems by peptides similar or identical to EGF; and second, potentiation of these and subsequent cellular events by the combined action of insulin plus glucagon. [Amiloride: N-amidino-3,5-diamino-6-chloropyrazinecarboxamide; furosemide: 4-chloro-N-furfuryl-5-sulfamoylanthranilic acid; AIB: alpha-aminoisobutyric acid; ID50: administered dose giving 50% inhibition of a maximal response; dFBS: dialyzed fetal bovine serum; L.I.: 3H-dT nuclear labeling index.]
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=509519&dopt=Abstract
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