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Regulation of the atrial muscarinic ...

Pleumsamran, Apisate.

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Regulation of the atrial muscarinic potassium channel by GTP-binding protein and adenosine-5'-triphosphate.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Regulation of the atrial muscarinic potassium channel by GTP-binding protein and adenosine-5'-triphosphate./
Author:	Pleumsamran, Apisate.
Description:	91 p.
Notes:	Source: Dissertation Abstracts International, Volume: 59-07, Section: B, page: 3166.
Contained By:	Dissertation Abstracts International59-07B.
Subject:	Biology, Animal Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9839277
ISBN:	0591929260

Regulation of the atrial muscarinic potassium channel by GTP-binding protein and adenosine-5'-triphosphate.
Pleumsamran, Apisate.

Regulation of the atrial muscarinic potassium channel by GTP-binding protein and adenosine-5'-triphosphate. - 91 p.

Source: Dissertation Abstracts International, Volume: 59-07, Section: B, page: 3166.

Thesis (Ph.D.)--The Herman M. Finch University of Health Sciences - The Chicago Medical School, 1998.

Acetylcholine (ACh) binds to the muscarinic receptors of pacemaker and atrial cells and activates an inwardly rectifying K

ISBN: 0591929260Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Regulation of the atrial muscarinic potassium channel by GTP-binding protein and adenosine-5'-triphosphate.
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035 $a (UnM)AAI9839277
035 $a AAI9839277
040 $a UnM $c UnM
100 1 $a Pleumsamran, Apisate. $3 1907163
245 1 0 $a Regulation of the atrial muscarinic potassium channel by GTP-binding protein and adenosine-5'-triphosphate.
300 $a 91 p.
500 $a Source: Dissertation Abstracts International, Volume: 59-07, Section: B, page: 3166.
500 $a Adviser: Donghee Kim.
502 $a Thesis (Ph.D.)--The Herman M. Finch University of Health Sciences - The Chicago Medical School, 1998.
520 $a Acetylcholine (ACh) binds to the muscarinic receptors of pacemaker and atrial cells and activates an inwardly rectifying K $\ sp+ $ current via a pertussis toxin-sensitive guanosine-5 $\ sp\prime $- triphosphate (GTP)-binding protein. Recent studies in isolated membrane patches showed that intracellular adenosine-5 $\ sp\prime $- triphosphate (ATP) increased the channel open probability $\ sim $5 fold above the level produced by maximal stimulation of the G-protein. Therefore, it was hypothesized that intracellular ATP was also important in physiological activation and/or modulation of the muscarinic K $\ sp+ $ ( $\ rm K\sb{ACh} $) channels. In this study, I examined the effect of ATP on the $\ rm K\sb{ACh} $ channel in more detail and tested the hypothesis that ATP-dependent mechanism was involved in the $\ rm K\sb{ACh} $ current activation by ACh.
520 $a The role of ATP on $\ rm K\sb{ACh} $ current was studied in rat atrial cells using the patch-clamp technique. In the presence of ACh in the pipette, ATP applied with GTP to the cytoplasmic side of the inside-out patches increased the $\ rm K\sb{ACh} $ channel activity $\ sim $5 fold above the level obtained by GTP alone. The relation between channel activity and ATP concentration could be described by the Hill equation with a Hill coefficient of 1.7 and a half-maximal activation concentration of 15 $\ mu $5 \sp\prime $- triphosphate (UTP), a substrate of nucleoside diphosphate kinase (NDPK), could mimic the ATP effect. After activation by ACh, whole-cell $\ rm K\sb{ACh} $ current declined rapidly (fast desensitization) to 65% of the initial peak current. The involvement of ATP in the $\ rm K\sb{ACh} $ current activation by ACh was studied by measuring the whole-cell $\ rm K\sb{ACh} $ current after the reduction of intracellular ATP. In the presence of intracellular GTP, lowering intracellular ATP concentration decreased the peak and the steady-state $\ rm K\sb{ACh} $ current by 58% and 47% respectively. Replacing intracellular ATP with AMP-PNP or UTP did not prevent the reduction of $\ rm K\sb{ACh} $ current, suggesting that ATP hydrolysis was required for ACh to maximally activate the current. However, protein kinase inhibitors, staurosporine, H-7, or H-89, did not block the ATP effect. These results show that both G-protein and ATP-mediated pathways are important in the $\ rm K\sb{ACh} $ current activation by ACh in atrial cells.
590 $a School code: 0044.
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Chemistry, Biochemistry. $3 1017722
690 $a 0433
690 $a 0487
710 2 0 $a The Herman M. Finch University of Health Sciences - The Chicago Medical School. $3 1033524
773 0 $t Dissertation Abstracts International $g 59-07B.
790 1 0 $a Kim, Donghee, $e advisor
790 $a 0044
791 $a Ph.D.
792 $a 1998
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9839277