Evidence for two mechanisms of depolarization associated with alpha 1-adrenoceptor activation in the rat anococcygeus muscle
Membrane potential responses in the rat isolated anococcygeus to bath-applied noradrenaline and field stimulation have been investigated by use of intracellular microelectrode and combined extracellular electrical and mechanical (sucrose gap) recording techniques. Intracellular recordings were made...
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Published in | British journal of pharmacology Vol. 86; no. 3; pp. 711 - 721 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
England
01.11.1985
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Abstract | Membrane potential responses in the rat isolated anococcygeus to bath-applied noradrenaline and field stimulation have been investigated by use of intracellular microelectrode and combined extracellular electrical and mechanical (sucrose gap) recording techniques. Intracellular recordings were made usually from tissues immobilized with hypertonic Krebs solution. Bath-application of noradrenaline produced depolarizations which consisted of two components; an initial 'fast' phase which peaked within 1-2 s and which was followed by a 'slow' sustained depolarization. Both components were concentration-dependent. Noradrenaline could also evoke oscillations in membrane potential which, unlike the 'fast' component of depolarization, were prevented by conditioning hyperpolarization of the membrane and were evoked by direct membrane depolarization with externally applied current pulses. Thus, the oscillations are voltage-dependent phenomena. Replacement of the external NaCl of the Krebs solution with an equimolar amount of Na benzenesulphonate abolished the noradrenaline-evoked 'fast' depolarization while the 'slow' phase was unaffected. This suggests that two mechanisms of depolarization are activated in this muscle by the bath-application of noradrenaline. The adrenergic excitatory junction potential was also abolished in Na benzenesulphonate. Prazosin reduced both the 'fast' and 'slow' components of depolarization produced by noradrenaline indicating their mediation by alpha 1-adrenoceptors. The membrane potential (-29 mV) at the maximum amplitude of the 'fast' depolarization was similar to the equilibrium potential (-27 mV) for the depolarization evoked by ionophoretically applied noradrenaline and which was obtained by extrapolation from the relationship between amplitude of the ionophoretic response and membrane potential displacement in the partition chamber. These results suggest that the 'fast' depolarization and the ionophoretic response are due to an increased membrane conductance, possibly to chloride. |
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AbstractList | Membrane potential responses in the rat isolated anococcygeus to bath‐applied noradrenaline and field stimulation have been investigated by use of intracellular microelectrode and combined extracellular electrical and mechanical (sucrose gap) recording techniques. Intracellular recordings were made usually from tissues immobilized with hypertonic Krebs solution.
Bath‐application of noradrenaline produced depolarizations which consisted of two components; an initial ‘fast’ phase which peaked within 1–2 s and which was followed by a ‘slow’ sustained depolarization. Both components were concentration‐dependent.
Noradrenaline could also evoke oscillations in membrane potential which, unlike the ‘fast’ component of depolarization, were prevented by conditioning hyperpolarization of the membrane and were evoked by direct membrane depolarization with externally applied current pulses. Thus, the oscillations are voltage‐dependent phenomena.
Replacement of the external NaCl of the Krebs solution with an equimolar amount of Na benzenesulphonate abolished the noradrenaline‐evoked ‘fast’ depolarization while the ‘slow’ phase was unaffected. This suggests that two mechanisms of depolarization are activated in this muscle by the bath‐application of noradrenaline. The adrenergic excitatory junction potential was also abolished in Na benzenesulphonate.
Prazosin reduced both the ‘fast’ and ‘slow’ components of depolarization produced by noradrenaline indicating their mediation by α
1
‐adrenoceptors.
The membrane potential (‐ 29 mV) at the maximum amplitude of the ‘fast’ depolarization was similar to the equilibrium potential (‐ 27 mV) for the depolarization evoked by ionophoretically applied noradrenaline and which was obtained by extrapolation from the relationship between amplitude of the ionophoretic response and membrane potential displacement in the partition chamber. These results suggest that the ‘fast’ depolarization and the ionophoretic response are due to an increased membrane conductance, possibly to chloride. Membrane potential responses in the rat isolated anococcygeus to bath-applied noradrenaline and field stimulation have been investigated by use of intracellular microelectrode and combined extracellular electrical and mechanical (sucrose gap) recording techniques. Intracellular recordings were made usually from tissues immobilized with hypertonic Krebs solution. Bath-application of noradrenaline produced depolarizations which consisted of two components; an initial 'fast' phase which peaked within 1-2 s and which was followed by a 'slow' sustained depolarization. Both components were concentration-dependent. Noradrenaline could also evoke oscillations in membrane potential which, unlike the 'fast' component of depolarization, were prevented by conditioning hyperpolarization of the membrane and were evoked by direct membrane depolarization with externally applied current pulses. Thus, the oscillations are voltage-dependent phenomena. Replacement of the external NaCl of the Krebs solution with an equimolar amount of Na benzenesulphonate abolished the noradrenaline-evoked 'fast' depolarization while the 'slow' phase was unaffected. This suggests that two mechanisms of depolarization are activated in this muscle by the bath-application of noradrenaline. The adrenergic excitatory junction potential was also abolished in Na benzenesulphonate. Prazosin reduced both the 'fast' and 'slow' components of depolarization produced by noradrenaline indicating their mediation by alpha 1-adrenoceptors. The membrane potential (-29 mV) at the maximum amplitude of the 'fast' depolarization was similar to the equilibrium potential (-27 mV) for the depolarization evoked by ionophoretically applied noradrenaline and which was obtained by extrapolation from the relationship between amplitude of the ionophoretic response and membrane potential displacement in the partition chamber. These results suggest that the 'fast' depolarization and the ionophoretic response are due to an increased membrane conductance, possibly to chloride. |
Author | Large, W A Byrne, N G |
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References | Bolton T.B. (e_1_2_1_5_1) 1985 e_1_2_1_7_1 Byrne N.G. (e_1_2_1_8_1) 1985; 360 e_1_2_1_20_1 e_1_2_1_6_1 e_1_2_1_3_1 e_1_2_1_12_1 e_1_2_1_23_1 e_1_2_1_4_1 e_1_2_1_13_1 e_1_2_1_24_1 e_1_2_1_10_1 e_1_2_1_21_1 e_1_2_1_2_1 e_1_2_1_11_1 e_1_2_1_22_1 e_1_2_1_16_1 e_1_2_1_17_1 e_1_2_1_14_1 e_1_2_1_15_1 e_1_2_1_9_1 e_1_2_1_18_1 e_1_2_1_19_1 |
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SubjectTerms | Anal Canal Animals Benzenesulfonates - pharmacology Chlorides - physiology Electric Stimulation In Vitro Techniques Iontophoresis Membrane Potentials - drug effects Muscle Contraction - drug effects Muscle, Smooth - drug effects Muscle, Smooth - physiology Norepinephrine - antagonists & inhibitors Norepinephrine - pharmacology Perfusion Prazosin - pharmacology Rats Receptors, Adrenergic, alpha - drug effects Receptors, Adrenergic, alpha - physiology Sacrococcygeal Region Sodium Chloride - pharmacology |
Title | Evidence for two mechanisms of depolarization associated with alpha 1-adrenoceptor activation in the rat anococcygeus muscle |
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