Coronary metabolic adaptation restricted by endothelin in the dog heart

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Abstract

Endothelin elicits long-lasting vasoconstriction in the coronary bed. This remarkable spastic response raises the question whether or not the metabolic adaptive mechanisms of the coronaries are activated under endothelin effect. The role of the compensatory mediators adenosine and inosine was investigated before and after intracoronary (ic.) administration of endothelin-1 (ET-1, 1.0 nmol) using 1-min reactive hyperemia (RH) tests on in situ dog hearts (n=15) with or without blocking the ATP-sensitive potassium (K+ATP) channels by glibenclamide (GLIB, 1.0 μmol min-1, ic.). The release of adenosine and inosine via the coronary sinus was measured by HPLC during the first minute of RH. Endothelin-1 reduced baseline coronary blood flow (CBF) and RH response (hyperemic excess flow (EF) control vs. ET-1: 81.7±13.6 vs. 43.4±10.9 ml, P

Original languageEnglish
Pages (from-to)35-46
Number of pages12
JournalActa Physiologica Hungarica
Volume88
Issue number1
DOIs
Publication statusPublished - 2001

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Endothelins
Hyperemia
Inosine
Endothelin-1
Dogs
Adenosine
KATP Channels
Muscle Spasticity
Coronary Sinus
Glyburide
Vasoconstriction
Adenosine Triphosphate
High Pressure Liquid Chromatography

ASJC Scopus subject areas

  • Physiology

Cite this

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abstract = "Endothelin elicits long-lasting vasoconstriction in the coronary bed. This remarkable spastic response raises the question whether or not the metabolic adaptive mechanisms of the coronaries are activated under endothelin effect. The role of the compensatory mediators adenosine and inosine was investigated before and after intracoronary (ic.) administration of endothelin-1 (ET-1, 1.0 nmol) using 1-min reactive hyperemia (RH) tests on in situ dog hearts (n=15) with or without blocking the ATP-sensitive potassium (K+ATP) channels by glibenclamide (GLIB, 1.0 μmol min-1, ic.). The release of adenosine and inosine via the coronary sinus was measured by HPLC during the first minute of RH. Endothelin-1 reduced baseline coronary blood flow (CBF) and RH response (hyperemic excess flow (EF) control vs. ET-1: 81.7±13.6 vs. 43.4±10.9 ml, P",
author = "L. Fazekas and V. K{\'e}kesi and P. So{\'o}s and E. Bar{\'a}t and E. Husz{\'a}r and A. Juh{\'a}sz-Nagy",
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T1 - Coronary metabolic adaptation restricted by endothelin in the dog heart

AU - Fazekas, L.

AU - Kékesi, V.

AU - Soós, P.

AU - Barát, E.

AU - Huszár, E.

AU - Juhász-Nagy, A.

PY - 2001

Y1 - 2001

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AB - Endothelin elicits long-lasting vasoconstriction in the coronary bed. This remarkable spastic response raises the question whether or not the metabolic adaptive mechanisms of the coronaries are activated under endothelin effect. The role of the compensatory mediators adenosine and inosine was investigated before and after intracoronary (ic.) administration of endothelin-1 (ET-1, 1.0 nmol) using 1-min reactive hyperemia (RH) tests on in situ dog hearts (n=15) with or without blocking the ATP-sensitive potassium (K+ATP) channels by glibenclamide (GLIB, 1.0 μmol min-1, ic.). The release of adenosine and inosine via the coronary sinus was measured by HPLC during the first minute of RH. Endothelin-1 reduced baseline coronary blood flow (CBF) and RH response (hyperemic excess flow (EF) control vs. ET-1: 81.7±13.6 vs. 43.4±10.9 ml, P

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EP - 46

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JF - Physiology International

SN - 2498-602X

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