Mechanisms involved in contraction of smooth muscles of the rat portal vein as induced by sodium depletion.

Yamamoto, Yasutake; Hotta, Ken

doi:10.2170/jjphysiol.35.717

Cited by 5 publications

(2 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The potential corresponding to half-activation, determined from the mean peak conductance curve obtained for the Ca2 + channel current recorded in the reference solution (Figure 4) was -5.7 + 0.3 mV (n = 3), a value 21 mV more negative than that obtained in 90mM Ba2+. The foot of the activation curve was -50 mV, a value that corresponds to the resting potential of portal vein cells (Nanjo, 1984;Yamamoto & Hotta, 1985). Taken together, these results suggest that NA could not induce a significant Ca2+ influx through voltage-dependent Ca2 channels if the membrane potential was maintained at -50 mV.…”

Section: Single-channel Recordingsmentioning

confidence: 66%

Ca²⁺ channel activation and membrane depolarization mediated by Cl⁻ channels in response to noradrenaline in vascular myocytes

Pacaud

Loirand

Baron

et al. 1991

British J Pharmacology

View full text Add to dashboard Cite

I The effects of noradrenaline (NA) were studied on vascular smooth muscle cells isolated from rat portal vein. 2 Two types of single-Ca2+ channel currents with conductances of 17pS and 8pS were obtained in cell-attached configuration. Bath application of NA increased the open probability of both channels during depolarizing pulses without a change of background membrane conductance. However, NA did not open Ca2 + channels when the membrane patch potential was held at -50mV, which is about the resting potential in physiological conditions. 3 In the whole-cell configuration, studies of voltage-dependent Ca2+ channel currents showed that the peak conductance curve was not shifted to more negative potentials by NA.4 Measurements of internal Ca2+-concentration ([Ca2+]) with Indo-1 indicated that NA increased [Ca2+] at a holding potential of -50 mV and evoked a Ca2 '-activated Cl-current. These effects were blocked when heparin was included in the pipette solution. 5 A Cl -channel blocker without effect on Ca2 + channels (anthracene-9-carboxylic acid) inhibited the contractions of portal vein strips induced by NA in a manner similar to that produced by a Ca2 + channel inhibitor (isradipine). The NA-induced contraction was completely suppressed in the presence of ryanodine which depletes intracellular Ca2 + stores. 6 The present study suggests that activation of Cl -channels by Ca2+ release produces a membrane depolarization which is a prerequisite for enhanced opening of voltage-dependent Ca2+ channels in response to NA in venous smooth muscle.

show abstract

Section: Single-channel Recordingsmentioning

confidence: 66%

Ca²⁺ channel activation and membrane depolarization mediated by Cl⁻ channels in response to noradrenaline in vascular myocytes

Pacaud

Loirand

Baron

et al. 1991

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…These results indicate that the relaxing effect of KCN may be much more sensitive to sucrose substitution compared with those of D 600 and papaverine. A possibility that calcium mobilizing pathways for K+-contracture would be altered in Na+-free media has been discussed in the rabbit ear artery (22), guinea pig mesenteric artery (23) and rat portal vein (24).…”

Section: Resultsmentioning

confidence: 99%

Effects of sucrose- or Tris-substitution for Na+ on responses to D 600, papaverine and KCN in the K+-depolarized taenia coli of guinea pigs.

et al. 1988

View full text Add to dashboard Cite

Abstract-Effects of D 600, papaverine and KCN on sustained contracture induced by 20 mM KCI in a Nat-free sucrose or Iris-substituted solution were investigated in the taenia coil of guinea pigs. D 600 (10-5 M) and papaverine (10-4 M), added after 40 min incubation in the 20 mM KCI sucrose solution, relaxed the muscle by 88.2±8.0% (mean±S.E., n=4) and 78.8±6.3% (n=4), respectively. In contrast to this, KCN (10-3 M) relaxed the muscle by 11.0±4.7% (n=4) after a 20 min incubation in the sucrose solution. The concentration-relaxation curves for these relaxants were slightly shifted to the right in the Na+-free 20 mM KCI Tris solution. The cellular Na+ content of the taenia coil was greatly reduced by exposure to the sucrose or Tris solution, while the Ca2+ contents in both solutions were gradually increased with the exposure time. When a glucose-free solution was applied 60 min after the KCI-induced sustained contracture, gradual relaxation in the normal solution was observed. This relaxation was completely inhibited in the Na+-free sucrose solution. These results suggest that the relaxing activities of the different inhibitors are changed to different degrees by the replacement of Na' with sucrose in the guinea-pig taenia coil and that sustained KCI-contracture in a Na+-free sucrose solution may be less energy-dependent as compared with that in a Na+-free Tris medium. These results also indicate the inability to directly correlate the changes in the Ca2+ and Na+ contents with the greatly reduced activities of the relaxants in a Nat-free sucrose solution.

show abstract

Regulation of vascular smooth muscle contraction by extracellular Na+

Rapoport

1993

General Pharmacology: The Vascular System

View full text Add to dashboard Cite

Mechanisms involved in contraction of smooth muscles of the rat portal vein as induced by sodium depletion.

Abstract: Responses to external Na depletion were investigated in the rat portal vein, using a microelectrode and an isometric force transducer.

Cited by 5 publications

References 16 publications

Ca²⁺ channel activation and membrane depolarization mediated by Cl⁻ channels in response to noradrenaline in vascular myocytes

Ca²⁺ channel activation and membrane depolarization mediated by Cl⁻ channels in response to noradrenaline in vascular myocytes

Effects of sucrose- or Tris-substitution for Na+ on responses to D 600, papaverine and KCN in the K+-depolarized taenia coli of guinea pigs.

Regulation of vascular smooth muscle contraction by extracellular Na+

Contact Info

Product

Resources

About

Mechanisms involved in contraction of smooth muscles of the rat portal vein as induced by sodium depletion.

Abstract: Responses to external Na depletion were investigated in the rat portal vein, using a microelectrode and an isometric force transducer.

Cited by 5 publications

References 16 publications

Ca2+ channel activation and membrane depolarization mediated by Cl− channels in response to noradrenaline in vascular myocytes

Ca2+ channel activation and membrane depolarization mediated by Cl− channels in response to noradrenaline in vascular myocytes

Effects of sucrose- or Tris-substitution for Na+ on responses to D 600, papaverine and KCN in the K+-depolarized taenia coli of guinea pigs.

Regulation of vascular smooth muscle contraction by extracellular Na+

Contact Info

Product

Resources

About

Ca²⁺ channel activation and membrane depolarization mediated by Cl⁻ channels in response to noradrenaline in vascular myocytes

Ca²⁺ channel activation and membrane depolarization mediated by Cl⁻ channels in response to noradrenaline in vascular myocytes