Key result
Intracellular alkalinization with NH4Cl potentiated inward Ca2+ channel currents and reduced peak intracellular Ca2+ during K+ contracture, while acidification with propionate had opposite effects.
Why the study?
Does modification of intracellular pH affect calcium currents and intracellular calcium ions in rabbit portal vein smooth muscle cells?
Does modification of intracellular pH affect calcium currents and intracellular calcium ions in rabbit portal vein smooth muscle cells?
The modification of Ca2+ channel currents by intracellular pH is not directly related to its effects on the mechanical response to excess K+, suggesting direct effects of pHi on [Ca2+]i and contractile machinery.
Answers are grounded in this paper and cite their sources.
pHi modulation of Ca2+ currents in rabbit vascular smooth muscle is hypothesis-generating; leaves open relevance to human vasomotor control.
In smooth muscle cells freshly dispersed from the rabbit portal vein, effects of intracellular pH (pHi) on Ca2+ channel currents were studied with the whole-cell clamp method using nystatin in the pipette. pHi was modified with ammonium chloride (NH4Cl) and propionate. Changes in intracellular Ca2+ concentration ([Ca2+]i) and pHi were also measured with the fluorescent indicator fura-2 and a pH-sensitive dye, respectively, together with the mechanical response in intact tissues. Intracellular alkalinization caused by an application of NH4Cl (20 mM) markedly potentiated and acidification caused by propionate (20 mM) inhibited inward Ca2+ channel currents, without much change in the kinetics. Tension development induced by 60 mM K- was inhibited by NH4Cl (20 mM) and potentiated by propionate (20 mM), whereas the peak [Ca2+]i level reached during K+ contracture was reduced in the presence of NH4Cl and increased in the presence of propionate. It was concluded that the modification of Ca2+ channel currents caused by pHi is not directly related to the effects of pHi on the mechanical response to excess K+. The direct effects of pHi on [Ca2+]i and on contractile machinery are considered to be mainly responsible for the mechanical effect of pHi.
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Iino et al. (1994) studied this question. Intracellular pH modification (NH4Cl and propionate) was evaluated on Ca2+ channel currents, intracellular Ca2+ concentration, and mechanical response. Intracellular alkalinization with NH4Cl potentiated inward Ca2+ channel currents and reduced peak intracellular Ca2+ during K+ contracture, while acidification with propionate had opposite effects.
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