Role of InsP3 and ryanodine receptors in the activation of capacitative Ca2+ entry by store depletion or hypoxia in canine pulmonary arterial smooth muscle cells.

Role of InsP3 and ryanodine receptors in the activation of capacitative Ca2+ entry by store depletion or hypoxia in canine pulmonary arterial smooth muscle cells. Research Abstract Details 

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Role of InsP3 and ryanodine receptors in the activation of capacitative Ca2+ entry by store depletion or hypoxia in canine pulmonary arterial smooth muscle cells. Abstract Text:

L C Ng,S M Wilson,C E McAllister,J R Hume,

BACKGROUND AND PURPOSE: Experiments were performed to determine if capacitative Ca(2+) entry (CCE) in canine pulmonary arterial smooth muscle cells (PASMCs) is dependent on InsP(3) receptors or ryanodine receptors as induction of CCE is dependent on simultaneous depletion of the functionally separate InsP(3)- and ryanodine-sensitive sarcoplasmic reticulum (SR) Ca(2+) stores in these cells. EXPERIMENTAL APPROACH: Myocytes were isolated from canine pulmonary arteries using enzymatic procedures and were used within 8 h of preparation. Measurements of cytosolic Ca(2+) were made by imaging fura-2 loaded individual myocytes that were perfused with physiological buffered saline solution with or without Ca(2+). KEY RESULTS: Treating myocytes with 10 microM cyclopiazonic acid (CPA), removing extracellular Ca(2+), and briefly applying 10 mM caffeine and 10 microM 5-hydroxytryptamine (5-HT) depleted SR Ca(2+) stores. Extracellular Ca(2+) reintroduction caused cytosolic [Ca(2+)] to elevate above baseline signifying CCE. The InsP(3) receptor inhibitors 2-aminobiphenylborate (50-75 microM; 2-APB) and xestospongin-C (20 microM; XeC) abolished CCE. Yet, CCE was unaffected by 10 microM or 300 microM ryanodine or 10 microM dantrolene, which modify ryanodine receptor activity. Higher dantrolene concentrations (50 microM), however, can inhibit both ryanodine receptors and InsP(3) receptors, did reduce CCE. In contrast, CCE activated by hypoxia was unaffected by XeC (20 microM). CONCLUSIONS AND IMPLICATIONS: The results provide evidence that CCE activated by depletion of both InsP(3) and ryanodine SR Ca(2+) stores in canine PASMCs is dependent on functional InsP(3) receptors, whereas the activation of CCE by hypoxia appears to be independent of functional InsP(3) receptors.

Role of InsP3 and ryanodine receptors in the activation of capacitative Ca2+ entry by store depletion or hypoxia in canine pulmonary arterial smooth muscle cells. Publishing Authors By Initials

LC Ng,SM Wilson,CE McAllister,JR Hume,

For similar natural sciences: time: time factors research abstracts see: natural sciences: time: time factors research

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Role of InsP3 and ryanodine receptors in the activation of capacitative Ca2+ entry by store depletion or hypoxia in canine pulmonary arterial smooth muscle cells. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: British journal of pharmacology

VOLUME: 152

Page Numbers: 101-11

Journal Abbreviation: Br. J. Pharmacol.

ISSN: 0007-1188

DAY: 25

MONTH: 06

YEAR: 2007

Role of InsP3 and ryanodine receptors in the activation of capacitative Ca2+ entry by store depletion or hypoxia in canine pulmonary arterial smooth muscle cells. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7502536

Role of InsP3 and ryanodine receptors in the activation of capacitative Ca2+ entry by store depletion or hypoxia in canine pulmonary arterial smooth muscle cells. Keywords Mesh Terms:

KEYWORDS: Time Factors

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Role of InsP3 and ryanodine receptors in the activation of capacitative Ca2+ entry by store depletion or hypoxia in canine pulmonary arterial smooth muscle cells. Information

Substance Name: Calcium-Transporting ATPases

Registry Number: EC 3.6.1.8

Grant and Affiliation Information for Role of InsP3 and ryanodine receptors in the activation of capacitative Ca2+ entry by store depletion or hypoxia in canine pulmonary arterial smooth muscle cells.

AFFILIATION: Department of Pharmacology, University of Nevada School of Medicine, Reno, NV, USA.

Country: England

AGENCY: United States NCRR

GRANT: P20 RR 15518

ACRONYM: RR

MEDLINETA: Br J Pharmacol

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