Drugs online research references
J Membr Biol. 2001 Sep 15;183(2):93-101.
Cell signaling pathways mediating epidermal growth factor stimulation of Na:K:2Cl cotransport activity in rabbit corneal epithelial cells.
Yang H, Wang Z, Miyamoto Y, Reinach PS.
College of Optometry, Department of Biological Sciences, State University of New York, 33 W. 42nd Street, New York, NY 10036, USA.
We characterized the signaling and ion transport pathways that mediate epidermal growth factor receptor physiological control in SV40-immortalized rabbit corneal epithelial cells (tRCEC). Our evaluation employed single-cell fluorescence imaging to measure the intracellular [Na+]i in these cells loaded with the Na+ sensitive dye, SBFI. EGF (1 to 5 ng/ml) transiently increased [Na+]i from 10 mm to as much as 35 mm after 25 min, which was followed by a decline towards its control value. These increases waned at higher EGF concentrations up to 50 ng/ml. Both inhibition of EGF receptor-linked tyrosine kinase activity (50 microm RG-13022) and cPLA2 activity (10 microm AACOCF3) obviated EGF-induced increases in [Na+]i. In contrast, PGE2 (10 microg/ml) and cAMP (2 mm) increased [Na+]i by 25 mm. Inhibition of NKCC activity through exposure to either Cl-free Ringers or 300 microm furosemide in NaCl Ringers eliminated EGF-induced increases in [Na+]i. Similarly, EGF failed to increase [Na+]i following inhibition of: 1) PKA activity (10 microm H-89); 2) Erk1/2 (15 microm PD98059) or 3) p38 (15 microm SB203580) activity. Stimulation protein kinase C activity (0.1 microm PMA) transiently increased [Na+]i followed by a decline towards its baseline value. EGF-induced increases in [Na+]i were unaltered by inhibition of K+ conductance (100 microm 4-AP). Taken together, EGF stimulates Erk1/2; p38 and cPLA2 activity. Their stimulation increases PGE2 and cAMP levels resulting in PKA and NKCC activation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11562791&dopt=Abstract
J Physiol. 1978 Oct;283:121-32.
The blockade of GABA mediated responses in the frog spinal cord by ammonium ions and furosemide.
Nicoll RA.
1. A variety of compounds which are known to block chloride transport in a variety of systems have been examined for their effects on amino acid and synaptic responses in the frog spinal cord in vitro. 2. A number of monocarboxylic aromatic acids, copper sulphate, and acetazolamide had no effect on any of the responses. 3. Ammonium ions blocked the motoneurone hyperpolarizing responses to all the neutral amino acids. In addition it selectively blocked dorsal root potentials and the action of GABA and beta-alanine on primary afferents. 5. Intracellular recording from dorsal root ganglion cells demonstrated that furosemide had little effect on the reversal potential for the GABA response. These results suggest that furosemide acts primarily by blocking the conductance increase elicited by GABA. 6. The results with furosemide provide indirect evidence that chloride ions are involved in generating the GABA depolarizations of primary afferent terminals and dorsal root potentials.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=722571&dopt=Abstract
Laryngoscope. 1982 May;92(5):589-93.
Arguments against a mediating role of the adenylate cyclase--cyclic AMP system in the ototoxic action of loop diuretics.
Thalmann I, Kobayashi T, Thalmann R.
Previous studies in our laboratory have indicated that adenylate cyclase of the stria vascularis is strongly inhibited in vitro by ethacrynic acid and furosemide. In order to test whether the in vitro effects upon the enzyme are also present under in vivo conditions, ethacrynic acid was perfused perilymphatically for 15 min and 20 min at a concentration of 10(-3) M. Cyclic AMP of the stria vascularis was reduced by 27% and 34%, respectively, but ATP also declined significantly, suggesting unspecific effects. When ethacrynic acid was applied intravenously at a dosage of 50 mg/kg, and the endolymphatic potential allowed to decline to -10mV, no significant changes in cyclic AMP and ATP were seen. The absence of effects upon cyclic AMP in the early stage of systemic intoxication with ethacrynic acid is strong evidence against a mediating role of adenylate cyclase in the ototoxic action of ethacrynic acid. When a bolus of 3 x 10(-2) M furosemide was applied intra-arterially the endolymphatic potential declined at the exceedingly rapid rate of about 10 mV/sec, strongly suggesting that the action of the drug takes place in the vicinity of the capillaries of the stria vascularis. In view of the proposition that adenylate cyclase appears to be located primarily at eh luminal aspect of the stria vascularis, this constitutes further evidence against a role of the enzyme in the mediation of the specific ototoxic effects of loop diuretics. Other recent evidence against a mediatory role of the adenylate cyclase--cyclic AMP system is discussed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6281596&dopt=Abstract
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