Correlation between spontaneous electrical, calcium and mechanical activity in detrusor smooth muscle of the guinea‐pig bladder

To investigate the cellular mechanisms underlying spontaneous excitation of smooth muscle of the guinea‐pig urinary bladder, isometric tension was measured in muscle bundles while recording the membrane potential from a cell in the bundle with a microeletrode. Changes in the intracellular calcium co...

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Veröffentlicht in:British journal of pharmacology 2004-01, Vol.141 (1), p.183-193
Hauptverfasser: Hashitani, Hikaru, Brading, Alison F, Suzuki, Hikaru
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description To investigate the cellular mechanisms underlying spontaneous excitation of smooth muscle of the guinea‐pig urinary bladder, isometric tension was measured in muscle bundles while recording the membrane potential from a cell in the bundle with a microeletrode. Changes in the intracellular calcium concentration ([Ca2+]i; calcium transients) were recorded in strips loaded with the fluorescent dye, fura‐PE3. In 40% of preparations, individual action potentials and contractions, which were abolished by nifedipine (1 μM), were generated. In the remaining preparations, bursting action potentials and contractions were generated. Contractions were again abolished by nifedipine (1 μM), while higher concentrations of nifedipine (10–30 μM) were required to prevent the electrical activity. Carbachol (0.1 μM) increased the frequency of action potentials and corresponding contractions. Apamin (0.1 μM) potentiated bursting activity and enhanced phasic contraction. Charybdotoxin (CTX, 50 nM) induced prolonged action potentials that generated enlarged contractions. In contrast, levcromakalim (0.1 μM) reduced the frequency of action potentials, action potential bursts and the size of the contractions. Forskolin (0.1 μM), 8‐bromoguanosin 3′, 5′ cyclic monophosphate (8Br‐cGMP, 0.1 mM) and Y‐26763 (10 μM) suppressed contractions without reducing the amplitude of either action potentials or Ca transients. This paper confirms that action potentials and associated calcium transients are fundamental mechanisms in generating spontaneous contractions in smooth muscles of the guinea‐pig bladder. However, in parallel with the excitation–contraction coupling, the sensitivity of the contractile proteins for Ca2+ may play an important role in regulating spontaneous excitation and can be modulated by cyclic nucleotides and Rho kinase. British Journal of Pharmacology (2004) 141, 183–193. doi:10.1038/sj.bjp.0705602
doi_str_mv 10.1038/sj.bjp.0705602
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Changes in the intracellular calcium concentration ([Ca2+]i; calcium transients) were recorded in strips loaded with the fluorescent dye, fura‐PE3. In 40% of preparations, individual action potentials and contractions, which were abolished by nifedipine (1 μM), were generated. In the remaining preparations, bursting action potentials and contractions were generated. Contractions were again abolished by nifedipine (1 μM), while higher concentrations of nifedipine (10–30 μM) were required to prevent the electrical activity. Carbachol (0.1 μM) increased the frequency of action potentials and corresponding contractions. Apamin (0.1 μM) potentiated bursting activity and enhanced phasic contraction. Charybdotoxin (CTX, 50 nM) induced prolonged action potentials that generated enlarged contractions. In contrast, levcromakalim (0.1 μM) reduced the frequency of action potentials, action potential bursts and the size of the contractions. Forskolin (0.1 μM), 8‐bromoguanosin 3′, 5′ cyclic monophosphate (8Br‐cGMP, 0.1 mM) and Y‐26763 (10 μM) suppressed contractions without reducing the amplitude of either action potentials or Ca transients. This paper confirms that action potentials and associated calcium transients are fundamental mechanisms in generating spontaneous contractions in smooth muscles of the guinea‐pig bladder. However, in parallel with the excitation–contraction coupling, the sensitivity of the contractile proteins for Ca2+ may play an important role in regulating spontaneous excitation and can be modulated by cyclic nucleotides and Rho kinase. 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Forskolin (0.1 μM), 8‐bromoguanosin 3′, 5′ cyclic monophosphate (8Br‐cGMP, 0.1 mM) and Y‐26763 (10 μM) suppressed contractions without reducing the amplitude of either action potentials or Ca transients. This paper confirms that action potentials and associated calcium transients are fundamental mechanisms in generating spontaneous contractions in smooth muscles of the guinea‐pig bladder. However, in parallel with the excitation–contraction coupling, the sensitivity of the contractile proteins for Ca2+ may play an important role in regulating spontaneous excitation and can be modulated by cyclic nucleotides and Rho kinase. 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Changes in the intracellular calcium concentration ([Ca2+]i; calcium transients) were recorded in strips loaded with the fluorescent dye, fura‐PE3. In 40% of preparations, individual action potentials and contractions, which were abolished by nifedipine (1 μM), were generated. In the remaining preparations, bursting action potentials and contractions were generated. Contractions were again abolished by nifedipine (1 μM), while higher concentrations of nifedipine (10–30 μM) were required to prevent the electrical activity. Carbachol (0.1 μM) increased the frequency of action potentials and corresponding contractions. Apamin (0.1 μM) potentiated bursting activity and enhanced phasic contraction. Charybdotoxin (CTX, 50 nM) induced prolonged action potentials that generated enlarged contractions. In contrast, levcromakalim (0.1 μM) reduced the frequency of action potentials, action potential bursts and the size of the contractions. Forskolin (0.1 μM), 8‐bromoguanosin 3′, 5′ cyclic monophosphate (8Br‐cGMP, 0.1 mM) and Y‐26763 (10 μM) suppressed contractions without reducing the amplitude of either action potentials or Ca transients. This paper confirms that action potentials and associated calcium transients are fundamental mechanisms in generating spontaneous contractions in smooth muscles of the guinea‐pig bladder. However, in parallel with the excitation–contraction coupling, the sensitivity of the contractile proteins for Ca2+ may play an important role in regulating spontaneous excitation and can be modulated by cyclic nucleotides and Rho kinase. British Journal of Pharmacology (2004) 141, 183–193. doi:10.1038/sj.bjp.0705602</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>14662721</pmid><doi>10.1038/sj.bjp.0705602</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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subjects action potential
Action Potentials - drug effects
Action Potentials - physiology
Amides - pharmacology
Animals
Apamin - pharmacology
Biological and medical sciences
Boron Compounds - pharmacology
Ca sensitivity
Calcium - chemistry
Calcium - physiology
Calcium Signaling - physiology
Carbachol - pharmacology
Charybdotoxin - pharmacology
Colforsin - pharmacology
Cromakalim - pharmacology
Cyclic GMP - analogs & derivatives
Cyclic GMP - pharmacology
cyclic nucleotide
Dose-Response Relationship, Drug
Drug Synergism
Female
Fura-2
Guinea Pigs
Isotonic Contraction - drug effects
Isotonic Contraction - physiology
Male
Mechanotransduction, Cellular - physiology
Medical sciences
Microelectrodes
Muscle Contraction - drug effects
Muscle, Smooth - drug effects
Muscle, Smooth - physiology
Nifedipine - pharmacology
Pharmacology. Drug treatments
Pyridines - pharmacology
Transducers
Urinary bladder
Urinary Bladder - cytology
Urinary Bladder - drug effects
Urinary Bladder - physiology
title Correlation between spontaneous electrical, calcium and mechanical activity in detrusor smooth muscle of the guinea‐pig bladder
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