Abstract
The effects of arachidonic acid (AA) and its metabolites on the conductance (g(j)) of the gap junctions between neonatal rat myocardial cells was investigated. AA reduced g(j) in a dose- (2, 5, and 20 μM) and time- dependent fashion. Pretreatment of the cells with an inhibitor of the 5- lipoxygenase pathway, U-70344A, shifted the dose-response curve to the right; pretreatment with indomethacin, an inhibitor of the cyclooxygenase pathway, had no effect. The mean time to uncoupling was 3.7 ± 0.3, 3.8 ± 0.9, and 4.6 ± 0.6 min (means ± SE, P < 0.05) for 5 μM AA, 5 μM AA + indomethacin, and 5 μM AA + U-70344A, respectively. Incorporation of AA into membrane phospholipids was not affected by the inhibitor. These studies suggest that complete uncoupling of the cells occurred at membrane concentrations of 3-4 mol%. The data indicate that AA and a 5-lipoxygenase metabolite uncouple neonatal rat heart cells. The data are discussed with respect to the possible underlying mechanism of uncoupling and the potential role of gap junctions in arrhythmia formation in ischemic heart disease.
| Original language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Cell Physiology |
| Volume | 263 |
| Issue number | 2 32-2 |
| State | Published - 1992 |
Fingerprint
Keywords
- arrhythmia
- gap junctions
- heart
- intercellular communication
ASJC Scopus subject areas
- Clinical Biochemistry
- Cell Biology
- Physiology
Cite this
Arachidonic acid and lipoxygenase metabolites uncouple neonatal rat cardiac myocyte pairs. / Massey, K. D.; Minnich, B. N.; Burt, Janis M.
In: American Journal of Physiology - Cell Physiology, Vol. 263, No. 2 32-2, 1992.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Arachidonic acid and lipoxygenase metabolites uncouple neonatal rat cardiac myocyte pairs
AU - Massey, K. D.
AU - Minnich, B. N.
AU - Burt, Janis M
PY - 1992
Y1 - 1992
N2 - The effects of arachidonic acid (AA) and its metabolites on the conductance (g(j)) of the gap junctions between neonatal rat myocardial cells was investigated. AA reduced g(j) in a dose- (2, 5, and 20 μM) and time- dependent fashion. Pretreatment of the cells with an inhibitor of the 5- lipoxygenase pathway, U-70344A, shifted the dose-response curve to the right; pretreatment with indomethacin, an inhibitor of the cyclooxygenase pathway, had no effect. The mean time to uncoupling was 3.7 ± 0.3, 3.8 ± 0.9, and 4.6 ± 0.6 min (means ± SE, P < 0.05) for 5 μM AA, 5 μM AA + indomethacin, and 5 μM AA + U-70344A, respectively. Incorporation of AA into membrane phospholipids was not affected by the inhibitor. These studies suggest that complete uncoupling of the cells occurred at membrane concentrations of 3-4 mol%. The data indicate that AA and a 5-lipoxygenase metabolite uncouple neonatal rat heart cells. The data are discussed with respect to the possible underlying mechanism of uncoupling and the potential role of gap junctions in arrhythmia formation in ischemic heart disease.
AB - The effects of arachidonic acid (AA) and its metabolites on the conductance (g(j)) of the gap junctions between neonatal rat myocardial cells was investigated. AA reduced g(j) in a dose- (2, 5, and 20 μM) and time- dependent fashion. Pretreatment of the cells with an inhibitor of the 5- lipoxygenase pathway, U-70344A, shifted the dose-response curve to the right; pretreatment with indomethacin, an inhibitor of the cyclooxygenase pathway, had no effect. The mean time to uncoupling was 3.7 ± 0.3, 3.8 ± 0.9, and 4.6 ± 0.6 min (means ± SE, P < 0.05) for 5 μM AA, 5 μM AA + indomethacin, and 5 μM AA + U-70344A, respectively. Incorporation of AA into membrane phospholipids was not affected by the inhibitor. These studies suggest that complete uncoupling of the cells occurred at membrane concentrations of 3-4 mol%. The data indicate that AA and a 5-lipoxygenase metabolite uncouple neonatal rat heart cells. The data are discussed with respect to the possible underlying mechanism of uncoupling and the potential role of gap junctions in arrhythmia formation in ischemic heart disease.
KW - arrhythmia
KW - gap junctions
KW - heart
KW - intercellular communication
UR - http://www.scopus.com/inward/record.url?scp=0026671079&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0026671079&partnerID=8YFLogxK
M3 - Article
C2 - 1514593
AN - SCOPUS:0026671079
VL - 263
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6143
IS - 2 32-2
ER -