Glutamate receptor channels are ubiquitous agonist-gated channels. Pharmacologically they are classified into several subtypes but may have common fundamental channel properties. To build foundation for future molecular biological and genetic studies, we studied kinetics of the glutamate receptor channel in embryonic Drosophila myotubes in culture using the patch clamp technique. There were many brief lasting channel events together with prolonged ones. Brief events were frequently observed in low concentrations whereas the frequency of prolonged events increased with agonist concentrations. Long openings (> 5 ms) were often interrupted by brief closures, most of which lasted less than 100 mu s, thus showing a bursting behavior. At all agonist concentrations, the burst duration was fitted with three exponential components (brief, intermediate and long). The mean duration of the long component increased linearly with the glutamate concentration. The mean closed time and number of brief closures per ms within long bursts were independent of agonist concentration. The mean burst durations of the brief (30-250 mu s) and intermediate component (300-1050 mu s) did not change significantly with agonist concentration. The closing episodes within bursts were rare in the brief and intermediate burst components. The ratio of the fractional areas of the brief or intermediate and long burst components increased linearly with agonist concentration in the log-log plot with a slope of one. These findings suggest that the brief and intermediate components are due to singly-liganded openings and the long component is the result of doubly-liganded openings.
A numerical model of the rat distal tubule was developed to simulate water and solute transport in this nephron segment. This model incorporates the following: 1) Na-Cl cotransporter, K-Cl cotransporter, Na channel, K channel, and Cl channel in the luminal membrane; 2) Na-K-ATPase, K channel, and Cl channel in the basolateral membrane; and 3) conductances for Na, K, and Cl in the paracellular pathway. Transport rates were calculated using kinetic equations. Axial heterogeneity was represented by partitioning the model into two subsegments with different sets of model parameters. Model equations derived from the principles of mass conservation and electrical neutrality were solved numerically. Values of the model parameters were adjusted to minimize a penalty function that was devised to quantify the difference between model predictions and experimental results. The developed model could simulate the water and solute transport of the distal tubule in the normal state, as well as in conditions including thiazide or amiloride application and various levels of sodium load and tubular flow rate.
In the present study, we tested the direct effects of endothelin (ET) on rat kidney in vivo. ET was infused into the left renal artery of anesthetized rats at a rate of 0.5, 5, 20, or 40 pmol/h. ET reduced ipsilateral urine volume (V), clearance of inulin (CIN), and clearance of p-aminohippuric acid (CPAH) in a dose-dependent manner. Thus ET at 20 pmol/h did not change V but decreased renal plasma flow (RPF) and glomerular filtration rate (GFR) by 27.6 +/- 14.3 and 30.8 +/- 10.4%, respectively, in the ipsilateral kidney. ET at 0.5 pmol/h was without effect and at 5 pmol/h had only minor effects on CIN and CPAH of ipsilateral kidney. At 40 pmol/h, ET reduced ipsilateral V, GFR, and RPF by 52.3 +/- 21.4, 58.4 +/- 14.5, and 72.5 +/- 10.6%, respectively. Filtration fraction and fractional excretion of Na remained unchanged during ET infusion. ET, 40 pmol/h, infused into the renal artery together with atrial natriuretic peptide (ANP) at a rate of 12 pmol/h reduced the ipsilateral V, GFR, and RPF by 33.2 +/- 6.3, 26.1 +/- 6.0, and 27.2 +/- 7.1%, respectively, decrements less than those with ET alone. When a calcium-channel blocker nicardipine was infused at a rate of 2.5 micrograms/h into the renal artery together with ET, 20 pmol/h, there was little change in the ipsilateral V, RPF, and GFR; ET, 40 pmol/h, with nicardipine did not change V and decreased GFR and RPF by 25.9 +/- 5.6 and 23.1 +/- 10.8%, respectively, decrements less than those without nicardipine.(ABSTRACT TRUNCATED AT 250 WORDS)
Letters to the Editor are considered for publication (subject to editing and abridgment), provided they are submitted in duplicate, are typewritten and triple-spaced, and do not exceed 400 words of text, a maximum of five references, and one figure or table. Letters should have no more than three authors, and all should sign the letter. Please include a word count, your telephone number, and your fax number (if available).Letters should not duplicate similar material being submitted or published elsewhere, and they should not contain abbreviations. Financial associations or other possible conflicts of interest should always be disclosed. Submission of a letter constitutes permission for the Massachusetts Medical Society, its licensees, and its assignees to use it in the Journal 's various editions (print, data base, and optical disk), in anthologies, revisions, and any other form or medium.Letters referring to a recent Journal article must be received within four weeks of the article's publication. To expedite receipt of such letters, we encourage authors outside the United States to communicate by fax (617-739-9864 or 617-734-4457).The Journal accepts letters to the Editor by electronic mail. The Internet address is letters@edit.nejm.org. We are unable to provide prepublication proofs, and unpublished material will not be returned to authors unless a stamped, self-addressed envelope is enclosed. Receipt of letters is not acknowledged, but correspondents will be notified when a decision is made.The New England Journal of Medicine Downloaded from nejm.org on August 12, 2015. For personal use only. No other uses without permission.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.