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Morphine induces an intracellular alkalinization in bovine aortic endothelial cells (BAECs).

Juliann Gong Kiang, Margaret Colden‐Stanfield

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Abstract

The resting intracellular pH (pHi) of BAECs, by using BCECF fluorescence, at 37 degrees C in Na+ Hanks' was 7.22 +/- 0.03. Cells which had been acid-loaded recovered from the intracellular acidification in Na+ Hanks' in a [Na+]o-dependent and amiloride-sensitive manner. Recovery from acidification had an apparent Km for Na+ of 40 +/- 10 mM and Ki for amiloride of 26 +/- 4 microM. Morphine (50 microM, 20 min, 37 degrees C) increased the pHi to 7.55 +/- 0.05. Naloxone (50 microM) given 5 min before morphine (50 microM) blocked this effect, indicating that this was an opiate receptor-mediated phenomenon. To determine if morphine activated the Na+/H+ exchanger, pHi was monitored in Na+-free Hanks', acidic Na+ Hanks' or amiloride-containing Na+ Hanks'. The alkalinization produced by morphine was not observed under all these circumstances. These data suggest morphine activates the Na+/H+ exchanger via opiate receptors.

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The resting intracellular pH (pHi) of BAECs, by using BCECF fluorescence, at 37 degrees C in Na+ Hanks' was 7.22 +/- 0.03. Cells which had been acid-loaded recovered from the intracellular acidification in Na+ Hanks' in a [Na+]o-dependent and amiloride-sensitive manner. Recovery from acidification had an apparent Km for Na+ of 40 +/- 10 mM and Ki for amiloride of 26 +/- 4 microM. Morphine (50 microM, 20 min, 37 degrees C) increased the pHi to 7.55 +/- 0.05. Naloxone (50 microM) given 5 min before morphine (50 microM) blocked this effect, indicating that this was an opiate receptor-mediated phenomenon. To determine if morphine activated the Na+/H+ exchanger, pHi was monitored in Na+-free Hanks', acidic Na+ Hanks' or amiloride-containing Na+ Hanks'. The alkalinization produced by morphine was not observed under all these circumstances. These data suggest morphine activates the Na+/H+ exchanger via opiate receptors.

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Available abstract

The resting intracellular pH (pHi) of BAECs, by using BCECF fluorescence, at 37 degrees C in Na+ Hanks' was 7.22 +/- 0.03. Cells which had been acid-loaded recovered from the intracellular acidification in Na+ Hanks' in a [Na+]o-dependent and amiloride-sensitive manner. Recovery from acidification had an apparent Km for Na+ of 40 +/- 10 mM and Ki for amiloride of 26 +/- 4 microM. Morphine (50 microM, 20 min, 37 degrees C) increased the pHi to 7.55 +/- 0.05. Naloxone (50 microM) given 5 min before morphine (50 microM) blocked this effect, indicating that this was an opiate receptor-mediated phenomenon. To determine if morphine activated the Na+/H+ exchanger, pHi was monitored in Na+-free Hanks', acidic Na+ Hanks' or amiloride-containing Na+ Hanks'. The alkalinization produced by morphine was not observed under all these circumstances. These data suggest morphine activates the Na+/H+ exchanger via opiate receptors.

Key concepts: Amiloride, Intracellular pH, Sodium–hydrogen antiporter, Morphine, Chemistry, Intracellular, (+)-Naloxone, Sodium

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Morphine induces an intracellular alkalinization in bovine aortic endothelial cells (BAECs). — Research Paper | ScholarLens