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Tytuł pozycji:

Beta-adrenergic and muscarinic regulation of the chloride current in guinea-pig ventricular cells.

Tytuł:
Beta-adrenergic and muscarinic regulation of the chloride current in guinea-pig ventricular cells.
Autorzy:
Tareen FM; Department of Physiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Ono K
Noma A
Ehara T
Źródło:
The Journal of physiology [J Physiol] 1991; Vol. 440, pp. 225-41.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: Oxford : Blackwell : Cambridge Univ. Press
Original Publication: London, Cambridge Univ. Press.
MeSH Terms:
Acetylcholine/*pharmacology
Adrenergic beta-Agonists/*pharmacology
Chlorides/*metabolism
Ion Channel Gating/*drug effects
Myocardium/*metabolism
Animals ; Cells, Cultured ; Colforsin/pharmacology ; Cyclic AMP/pharmacology ; Dose-Response Relationship, Drug ; Electrophysiology ; Epinephrine/antagonists & inhibitors ; Epinephrine/pharmacology ; Guinea Pigs ; Heart Ventricles/metabolism ; In Vitro Techniques
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Substance Nomenclature:
0 (Adrenergic beta-Agonists)
0 (Chlorides)
1F7A44V6OU (Colforsin)
E0399OZS9N (Cyclic AMP)
N9YNS0M02X (Acetylcholine)
YKH834O4BH (Epinephrine)
Entry Date(s):
Date Created: 19910101 Date Completed: 19920507 Latest Revision: 20190510
Update Code:
20240104
PubMed Central ID:
PMC1180149
DOI:
10.1113/jphysiol.1991.sp018705
PMID:
1687150
Czasopismo naukowe
1. Single guinea-pig ventricular cells were voltage clamped using the patch clamp method combined with the pipette-perfusion technique. The voltage-dependent current systems were mostly blocked, and the background membrane conductance was measured by applying ramp pulses. 2. beta-Adrenergic effectors and related substances such as adrenaline, isoprenaline, forskolin or internal application of cyclic AMP induced a current component which showed a reversal potential near the expected Cl- equilibrium potential as well as an outward rectification in the I-V relation. It is suggested that the activation of this Cl- current was due to phosphorylation of the channel protein or related structure by the cyclic AMP-dependent protein kinase. Coincidentally with the activation of the Cl- current, the membrane capacitance of the cell decreased reversibly. 3. Acetylcholine (ACh) depressed the responses induced by beta-adrenergic stimulation and forskolin, but failed to interfere with the one induced by cyclic AMP. 4. The dose dependence of the Cl- current activation by isoprenaline or forskolin was fitted by the Hill equation, with a coefficient of 1.9 and a half-maximum concentration K 1/2 = 13 nM for isoprenaline, and with a Hill coefficient of 3 and a K 1/2 = 1.2 microM for forskolin. In the presence of 5.5 microM-ACh the dose-response relation shifted to higher doses; K 1/2 was 65 nM for isoprenaline and 3.6 microM for forskolin. 5. Washing out ACh in the presence of isoprenaline frequently caused transient overshoots of the response. When a saturating concentration of isoprenaline was used, this rebound was not observed. 6. The internal application of cyclic GMP enhanced the response of the Cl- current induced by isoprenaline or adrenaline. 7. When cyclic AMP was applied internally, the response was small in most cells. When the cell was superfused with 20 microM-IBMX (3-isobutyl-1-methylxanthine), the Cl- current was consistently induced by the application of cyclic AMP. It is suggested that phosphodiesterase activity strongly buffered the influx of cyclic AMP through the patch pipette tip. 8. We suggest that the compensatory interaction between the beta-adrenergic stimulation and the muscarinic inhibition is at the membrane level, most probably via GTP-binding proteins in activating adenylate cyclase.

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