Calcium and Sodium Channels in Spontaneously Contracting Vascular Muscle Cells

Sturek, Michael; Hermsmeyer, Kent

doi:10.1126/science.2425434

Cited by 170 publications

(81 citation statements)

References 25 publications

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“…Recently, an l.v.a. Ca2+ current sensitive to holding potential, carried by Ca2+ and Ba2+ ions, has also been reported in heart cells (Bean, 1985;Nilius, Hess, Lansman & Tsien, 1985;Mitra & Morad, 1986), twitch muscle fibres (Cota & Stefani, 1986), rat myoballs (Cognard, Lazdunski & Romey, 1986) and in vascular smooth muscle cells (Sturek & Hermsmeyer, 1986). …”

Section: Separation Of Lva Currentsmentioning

confidence: 99%

Kinetics and selectivity of a low‐voltage‐activated calcium current in chick and rat sensory neurones.

Carbone

Lux

1987

The Journal of Physiology

405

221

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SUMMARY1. Using the whole-cell recording mode of the patch-clamp technique, we have investigated kinetic and selectivity properties of a low-voltage-activated (l.v.a.) Ca2+ current in chick and rat dorsal root ganglion (d.r.g.) neurones.2. L.v.a currents were activated at about -50 mV and reached maximum amplitudes between -30 and -20 mV with averages of -0-16 nA in chick and -03 nA in rat d.r.g. cells with 5 mM-extracellular Ca2+. Between -60 and -20 mV, the time to peak, tp, of this current decreased with increasing membrane depolarizations. An e-fold change of tp required a 14 mV potential change in chick and a 17 mV change in rat d.r.g. cells at 22 'C.3. Between -50 and + 20 mV inactivation of this current was fast, single exponential and voltage dependent. In rat, the time constant of inactivation, Th, was smaller and less voltage dependent than in chick.4. The amplitude of these currents increased by a factor of 5-10, when the extracellular Ca2+ concentration was changed from 1 to 95 mm. Amplitudes and kinetic parameters of the currents showed typical shifts along the voltage axis. No correlation between Ca2+ current amplitudes and activation-inactivation kinetics was found, suggesting that the reaction rates which control these processes are not dependent on Ca2+ entry. Recovery from inactivation was voltage dependent and developed with a timeconstant, Tr' in the order of 1 s. Tr was nearly halved by changing the potential from -80 to -120 mV.6. Tail currents associated with membrane repolarization were also voltage dependent and developed exponentially. Their time constant decreased by a factor of 3 when the potential was changed from -60 to -100 mV.7. A second and more prominent Ca2+ current was activated at potentials positive to -20 mV h.v.a.), masking the time course of l.v.a. currents. Between -20 and 0 mV, time to peak of the entire current increased by a factor of 2 but decreased again at higher membrane potentials. Inactivation also became significantly slower in this potential range.8. The contribution of the h.v.a. component to the total membrane current was

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Section: Separation Of Lva Currentsmentioning

confidence: 99%

Kinetics and selectivity of a low‐voltage‐activated calcium current in chick and rat sensory neurones.

Carbone

Lux

1987

The Journal of Physiology

405

221

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“…In the vascular muscles (rat mesentric artery [1]; rat portal verb [36]; dog saphenous vein [66]; cell line (A 10) from embryonic rat aorta [24]; primary culture of rat azygos vein [54]), evidence is presented for the existence of two different types of Ca channel. One type is activated by small depolarization ("low threshold") and inactivated relatively quickly ("fast" channels), and the other is activated by large depolarization ("high threshold") and inactivated relatively slowly ("slow" channels).…”

Section: Voltage-operated Ca Channelsmentioning

confidence: 99%

“…Na channel No clear evidence has been presented so far for the existence of Na channel in smooth muscles under the physiological condition, except for primary cultures of azygos venous muscle cells from neonatal rats [54]. In this cell, the inward current carried by Na was recorded under whole-cell clamp.…”

Section: Other Ionic Currentsmentioning

confidence: 99%

“…With these experimental conditions, the inward current was observed in several types of smooth muscle (rabbit urinary bladder [32]; longitudinal muscle of rabbit ileum [20,47,49,55,57]; guinea-pig taenia caeci [26]; guinea-pig and rabbit stomach [42]; toad and amphiuma stomach [18,19,64]; rat vas deferens [44]; rat mesenteric artery [1]; rabbit ear artery [21]; dog saphenous vein [66]; culture cell from embryonic rat aorta [24,62]; rat portal vein [36]; culture cell from neonatal rat azygos vein [54]. The inward current was not influenced by complete replacement of Na with equimolar TEA or tetramethylammonium (guinea-pig urinary bladder [32]), or Tris (with 50 mM TEA) (longitudinal muscle of rabbit ileum [49]).…”

Section: Voltage-operated Ca Channelsmentioning

confidence: 99%

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Ionic channels in smooth muscle studied with patch-clamp methods.

Tomita

1988

Jpn.J.Physiol

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“…Evidence has shown that, in vascular smooth muscle, action potentials are not dependent on Na + channels since tetrodotoxin (TTX) has no effect on amplitude and duration of action potentials [18], leading to the belief that these channels might not be present or prominent in these tissues. Nonetheless, Na + currents (I Na ) have been measured in visceral smooth muscles such as myometrium and uterus (pregnant), colon, esophagus, stomach, and ureter as well as in certain vascular smooth muscles such as the portal and azygos veins [2,8,[24][25][26]31,33,34]. The identification of functional voltage-gated Na + channels in quiescent and proliferating vascular smooth muscle cells (VSMC), however, has not been as forthcoming.…”

Section: Introductionmentioning

confidence: 99%

Identification of functional voltage-gated Na+ channels in cultured human pulmonary artery smooth muscle cells

Platoshyn

Remillard

Fantozzi

et al. 2005

Pflugers Arch - Eur J Physiol

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Electrical excitability, which plays an important role in excitation-contraction coupling in the pulmonary vasculature, is regulated by transmembrane ion flux in pulmonary artery smooth muscle cells (PASMC). This study aimed to characterize the electrophysiological properties and molecular identities of voltage-gated Na + channels in cultured human PASMC. We recorded tetrodotoxinsensitive and rapidly inactivating Na + currents with properties similar to those described in cardiac myocytes. Using RT-PCR, we detected transcripts of seven Na + channel α genes (SCN2A, 3A, 4A, 7A, 8A, 9A, and 11A), and two β subunit genes (SCN1B and 2B). Our results demonstrate that human PASMC express TTX-sensitive voltage-gated Na + channels. Their physiological functions remain unresolved, although our data suggest that Na + channel activity does not directly influence membrane potential, intracellular Ca 2+ release, or proliferation in normal human PASMC. Whether their expression and/or activity are heightened in the pathological state is discussed.Keywords membrane potential; Na + channels; vascular smooth muscle; pulmonary Voltage-gated Na + channels play a major role in regulating cell excitability, particularly as it pertains to the generation of action potentials in neurons, skeletal muscle, and cardiac myocytes. Evidence has shown that, in vascular smooth muscle, action potentials are not dependent on Na + channels since tetrodotoxin (TTX) has no effect on amplitude and duration of action potentials [18], leading to the belief that these channels might not be present or prominent in these tissues. Nonetheless, Na + currents (I Na ) have been measured in visceral smooth muscles such as myometrium and uterus (pregnant), colon, esophagus, stomach, and ureter as well as in certain vascular smooth muscles such as the portal and azygos veins [2,8,[24][25][26]31,33,34]. The identification of functional voltage-gated Na + channels in quiescent and proliferating vascular smooth muscle cells (VSMC), however, has not been as forthcoming. Currently, I Na have been measured in smooth muscle cells isolated from the coronary artery, aorta, vena cava, and pulmonary artery of various species, including humans [5,16,23,27]. On only rare occasions have I Na been recorded in freshly dissociated human VSMC, although they are readily detected when the same cells are cultured [28]. In isolated cases, I Na have been recorded in both freshly dispersed rabbit [27] de-differentiation and proliferation [28]. More specifically, voltage-gated Na + channel expression and activity may be required either to facilitate the transition or to promote the de-differentiation of cells from "contractile" to "synthetic" or "proliferative" phenotypes [20,30]. This raises the possibility that the expression of functional voltage-gated Na + channels in cultured cells act as a trigger for cell de-differentiation and proliferation, possibly via enhanced cytoplasmic free Ca 2+ concentration ([Ca 2+ ] cyt ).The molecular identification of the subunits that make ...

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Calcium and Sodium Channels in Spontaneously Contracting Vascular Muscle Cells

Cited by 170 publications

References 25 publications

Kinetics and selectivity of a low‐voltage‐activated calcium current in chick and rat sensory neurones.

Kinetics and selectivity of a low‐voltage‐activated calcium current in chick and rat sensory neurones.

Ionic channels in smooth muscle studied with patch-clamp methods.

Identification of functional voltage-gated Na+ channels in cultured human pulmonary artery smooth muscle cells

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