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Vanheel B, de Hemptinne A. Influence of KATP channel modulation on net potassium efflux from ischaemic mammalian cardiac tissue. Cardiovasc Res. 1992;26(11):1030-9doi: 10.1093/cvr/26.11.1030.
Vanheel, B., & de Hemptinne, A. (1992). Influence of KATP channel modulation on net potassium efflux from ischaemic mammalian cardiac tissue. Cardiovascular research, 26(11), 1030-9. https://doi.org/10.1093/cvr/26.11.1030
Vanheel, B, and de Hemptinne, A. "Influence of KATP channel modulation on net potassium efflux from ischaemic mammalian cardiac tissue." Cardiovascular research vol. 26,11 (1992): 1030-9. doi: https://doi.org/10.1093/cvr/26.11.1030
Vanheel B, de Hemptinne A. Influence of KATP channel modulation on net potassium efflux from ischaemic mammalian cardiac tissue. Cardiovasc Res. 1992 Nov;26(11):1030-9. doi: 10.1093/cvr/26.11.1030. PMID: 1291079.
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Cardiovasc Res. 1992 Nov;26(11):1030-9. doi: 10.1093/cvr/26.11.1030.

Influence of KATP channel modulation on net potassium efflux from ischaemic mammalian cardiac tissue.

Cardiovascular research

B Vanheel, A de Hemptinne

Affiliations

  1. Laboratory of Normal and Pathological Physiology, University of Gent, Belgium.

PMID: 1291079 DOI: 10.1093/cvr/26.11.1030

Abstract

OBJECTIVE: The aim was to investigate the effect of pre-exposure to inhibitors or activators of the ATP regulated K+ (KATP) channels on the ischaemia induced early changes of the extracellular K+ concentration, the extracellular pH, and the action potential in mammalian cardiac tissue.

METHODS: An in vitro model simulating ischaemia was applied to isolated guinea pig papillary muscles while simultaneous microelectrode measurements of the transmembrane potentials and of the pH and K+ activity at the surface of the preparation (pHs and asK respectively) were made.

RESULTS: During conditions of superfusion arrest, when accumulation of metabolic acids causes acidification of pHs, the simultaneous development of a true hypoxic state of the muscle is required in order to induce shortening of the action potential duration and accumulation of extracellular K+ with associated membrane depolarisation. Glibenclamide (10-50 microM) slowed the decrease of the action potential duration in 50% of the muscles, while the increase of asK was only moderately (approximately 20%) influenced. In the presence of 200 microM of the KATP channel inhibitor, the mean K+ accumulation was not significantly different from the control. The presence of tolbutamide (1 mM) had no effect on the decrease of action potential duration, but moderately slowed the increase of asK. Superfusion with lemakalim (BRL 38227) decreased action potential duration dose dependently. In papillary muscles in which action potential duration was shortened to approximately 60% of the control duration by presuperfusion with lemakalim, a subsequent ischaemic episode did not increase but rather delayed the rise in asK. During simulated ischaemia in the presence of Ba2+ ions (1 mM), asK showed a transient decrease followed by a rise at a rate similar to that in the absence of Ba2+.

CONCLUSIONS: Early ischaemic K+ accumulation and surface acidification are relatively insensitive to KATP channel inhibition or activation prior to the ischaemic insult. The rather loose coupling of the increase of asK and the decrease of action potential duration, as well as the limited effect of sulphonylureas on the K+ increase, suggests that mechanisms other than KATP channel opening could possibly contribute to the initial phase of ischaemic K+ accumulation.

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