Monday, January 14, 2008

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ang II sr induced /ca+2 release/Ca+2 cytosolic accessibility/afferent arteriole/ contraction relaxation of smooth muscle/sr making /Ca+2 accessible Am J Physiol Renal Physiol /294/F212-F219, Susan K. Fellner/William J. Arendshorst/08 with ryanodine (100 µM) and TMB-8 to block SR mobilization via the ryanodine receptor and inositol trisphosphate receptor, respectively

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Hope in dietary change for cures !!!

Since it is utterly impossible for me to see you in person I must continue to offer you information from our invention and allow it to assimilate and integrate data from the internet into pallatable pieces.
Here is the latest AMIE
Advanced Medical Informatics Education
Entry for the day 01-14-08

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ang II sr induced /ca+2 release/Ca+2 cytosolic accessibility/afferent arteriole/ contraction relaxation of smooth muscle/sr making /Ca+2 accessible Am J Physiol Renal Physiol /294/F212-F219, Susan K. Fellner/William J. Arendshorst/08 with ryanodine (100 µM) and TMB-8 to block SR mobilization via the ryanodine receptor and inositol trisphosphate receptor, respectively

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Abbreviation Abb_Known_As
SR Spiritual Realm
ensrd end stage reneal disease/component of SLE
psr phtotosensitive rash
src self reactive cells/MS path at cyte of myelin sheath
SRS/Robotic/term self reconfigurable system/
SRS/Robotic/term self reconfigurable system/Mtrain II/c 2 /DOF
ang II/SR angiotensin II/ see sarcoplasmic reticulum /Ca+2 involvement
Angiotensin II-stimulated Ca2+ entry mechanisms in afferent arterioles: role of transient receptor potential canonical channels and reverse Na+/Ca2+ exchange
Susan K. Fellner and William J. Arendshorst
Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina
Submitted 25 May 2007 ; accepted in final form 26 October 2007
In afferent arterioles, the signaling events that lead to an increase in cytosolic Ca2+ concentration ([Ca2+]i) and initiation of vascular contraction are increasingly being delineated. We have recently studied angiotensin II (ANG II)-mediated effects on sarcoplasmic reticulum (SR) mobilization of Ca2+ and the role of superoxide and cyclic adenosine diphosphoribose in these processes. In the current study we investigated the participation of transient receptor potential canonical channels (TRPC) and a Na+/Ca2+ exchanger (NCX) in Ca2+ entry mechanisms. Afferent arterioles, isolated with the magnetized polystyrene bead method, were loaded with fura-2 to measure [Ca2+]i ratiometrically. We observed that the Ca2+-dependent chloride channel blocker niflumic acid (10 and 50 µ M) affects neither the peak nor plateau [Ca2+]i response to ANG II. Arterioles were pretreated with ryanodine (100 µM) and TMB-8 to block SR mobilization via the ryanodine receptor and inositol trisphosphate receptor, respectively. The peak [Ca2+]i response to ANG II was reduced by 40%. Addition of 2-aminoethoxydiphenyl borane to block TRPC-mediated Ca2+ entry inhibited the peak [Ca2+]i ANG II response by 80% and the plateau by 74%. Flufenamic acid (FFA; 50 µM), which stimulates TRPC6, caused a sustained increase of [Ca2+]i of 146 nM. This response was unaffected by diltiazem or nifedipine. KB-R7943 (at the low concentration of 10 µM) inhibits reverse (but not forward) mode NCX. KB-R7943 decreased the peak [Ca2+]i response to ANG II by 48% and to FFA by 38%. We conclude that TRPC6 and reverse-mode NCX may be important Ca2+ entry pathways in afferent arterioles. renal microcirculation; voltage-gated calcium entry; vascular smooth muscle cell
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scle cns/renal normality/vasculiti skin lesions/malar rash nephrotic syndrome/esrd/cns activity Harrison 14th/ Vol 2/1875 Hahn,bh/90