The effect of pH on membrane electrical properties of vascular smooth muscle.

Persistent Link:
http://hdl.handle.net/10150/187098
Title:
The effect of pH on membrane electrical properties of vascular smooth muscle.
Author:
Liu, Bei-xing.
Issue Date:
1995
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
I have investigated the effect of changing extracellular pH (pH₀) with constant PCO₂ on the electrical and mechanical properties of vascular smooth muscle (VSM) in isolated guinea-pig mesenteric and femoral arteries. Acidosis depolarized the smooth muscle cells while alkalosis hyperpolarized the cells. Altering pH₀ also changed intracellular pH (pH(i)) in the same direction but to a smaller degree. Both the latency and half time of the changes in membrane potential (Vm) are much shorter than those of the changes in pH(i), indicating that change in pH₀ rather than change in pH(i) is primarily responsible for the change in Vm. Changing pH altered the time constant of the excitatory junction potential (EJP), which suggests that changing pH altered the membrane conductance of VSM. Application of glibenclamide and cromakalim did not significantly alter the effect of pH₀ on RMP, suggesting that ATP-regulated K channels or Ca-regulated K channels may not been affected by pH. Application of BaCl₂ inhibited alkalosis-induced membrane hyperpolarization and reduction of the EJP time constant, suggesting that alkalosis increases K current passing through inward rectifier potassium channels (I(K(i))). Vascular smooth muscle cells tended to repolarize somewhat toward their control level when the arteries were left in either acidic or alkaline buffers for 30 min. Application of 1 mM TEA inhibits this repolarization, suggesting that this repolarization may be due to the effect of secondary change in pH(i) or/and intracellular calcium ([Ca²⁺](i)) on Ca regulated K channels. I also found that lowering pH₀ elevated the threshold of the action potential evoked by perivascular stimulation of the mesenteric artery during application of 10 mM tetraethylammonium (TEA), while increasing pH₀ had the opposite effect. Lowering pH₀ increased the threshold of the action potential but increased the plateau duration of the action potential, while elevating pH₀ has the opposite effect. These results suggest that altering pH₀ affects Ca current through voltage-gated Ca channels. In conclusion, our studies are consistent rather with the hypothesis that changes in pH alter the threshold of voltage-gated Ca channels in vascular smooth muscle cells.
Type:
text; Dissertation-Reproduction (electronic)
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Physiological Sciences; Graduate College
Degree Grantor:
University of Arizona
Committee Chair:
Johnson, Paul C.

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleThe effect of pH on membrane electrical properties of vascular smooth muscle.en_US
dc.creatorLiu, Bei-xing.en_US
dc.contributor.authorLiu, Bei-xing.en_US
dc.date.issued1995en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractI have investigated the effect of changing extracellular pH (pH₀) with constant PCO₂ on the electrical and mechanical properties of vascular smooth muscle (VSM) in isolated guinea-pig mesenteric and femoral arteries. Acidosis depolarized the smooth muscle cells while alkalosis hyperpolarized the cells. Altering pH₀ also changed intracellular pH (pH(i)) in the same direction but to a smaller degree. Both the latency and half time of the changes in membrane potential (Vm) are much shorter than those of the changes in pH(i), indicating that change in pH₀ rather than change in pH(i) is primarily responsible for the change in Vm. Changing pH altered the time constant of the excitatory junction potential (EJP), which suggests that changing pH altered the membrane conductance of VSM. Application of glibenclamide and cromakalim did not significantly alter the effect of pH₀ on RMP, suggesting that ATP-regulated K channels or Ca-regulated K channels may not been affected by pH. Application of BaCl₂ inhibited alkalosis-induced membrane hyperpolarization and reduction of the EJP time constant, suggesting that alkalosis increases K current passing through inward rectifier potassium channels (I(K(i))). Vascular smooth muscle cells tended to repolarize somewhat toward their control level when the arteries were left in either acidic or alkaline buffers for 30 min. Application of 1 mM TEA inhibits this repolarization, suggesting that this repolarization may be due to the effect of secondary change in pH(i) or/and intracellular calcium ([Ca²⁺](i)) on Ca regulated K channels. I also found that lowering pH₀ elevated the threshold of the action potential evoked by perivascular stimulation of the mesenteric artery during application of 10 mM tetraethylammonium (TEA), while increasing pH₀ had the opposite effect. Lowering pH₀ increased the threshold of the action potential but increased the plateau duration of the action potential, while elevating pH₀ has the opposite effect. These results suggest that altering pH₀ affects Ca current through voltage-gated Ca channels. In conclusion, our studies are consistent rather with the hypothesis that changes in pH alter the threshold of voltage-gated Ca channels in vascular smooth muscle cells.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplinePhysiological Sciencesen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.chairJohnson, Paul C.en_US
dc.contributor.committeememberBaldwin, Ann L.en_US
dc.contributor.committeememberBurt, Janis M.en_US
dc.contributor.committeememberGillies, Robert J.en_US
dc.contributor.committeememberKeef, Kathleen D.en_US
dc.identifier.proquest9531118en_US
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