Electrical and mechanical properties of spontaneous contraction in hypertensive rat portal vein

Pflugers Arch - Eur J Physiol

Zou²,

Matsuda³

et al. 2000

Self Cite

The role of nitric oxide in the electrical and mechanical activities of the rat portal vein was examined in circular muscle preparations with intact endothelium that were isolated from the longitudinal muscle layer. In contrast to the longitudinal muscle preparation, the circular muscle preparation did not show spontaneous phasic contraction. Inhibition of nitric oxide synthesis by Nomega-nitro-L-arginine (L-NNA) induced a tonic contraction. The contraction was inhibited by L-arginine, sodium nitroprusside or nifedipine. L-NNA did not induce contraction in endothelium-damaged preparations. The membrane potential of smooth muscle cells recorded in endothelium-intact preparations showed sporadic action potentials. L-NNA increased the frequency of action potentials without changing the resting membrane potential. The action potentials were inhibited by nifedipine. In the presence of L-NNA, sodium nitroprusside decreased the frequency of the action potentials without changing the resting membrane potential. These results indicated that contraction of rat portal vein circular muscles is inhibited tonically by nitric oxide, at least partly through inhibition of electrical activity.

Section: Discussioncontrasting

confidence: 43%

Role of nitric oxide in the contraction of circular muscle in the rat portal vein

Pflugers Arch - Eur J Physiol

Zou²,

Matsuda³

et al. 2000

Self Cite

“…Membrane depolarization activates voltage-dependent Ca 2+ channels in isolated smooth muscle of rat portal vein [16] and the increase in intracellular Ca 2+ has been shown to involve activation of L-type Ca 2+ channels by membrane depolarization [12]. In the present study, the resting membrane potential of smooth muscle cells in the longitudinal smooth muscle layer was similar to that noted in a previous report on rat portal vein [22]. Action potential bursts appeared periodically and we observed an increase in the frequency of action potential bursts after the application of l-arginine.…”

Section: Discussionsupporting

confidence: 90%

“…Membrane potential was measured using a conventional microelectrode technique [22]. The adventitia-removed/endothelium-denuded longitudinal strips were mounted with the adventitial side up on a silicon rubber bed in a chamber perfused continuously with warmed Tyrode's solution at 5 ml/min.…”

Section: Methodsmentioning

confidence: 99%

Effects of l-arginine on spontaneous contraction of the rat portal vein

Pflugers Arch - Eur J Physiol

Zhou

Toba

et al. 2003

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The effects of L-arginine on spontaneous contraction of endothelium-denuded longitudinal preparations of the rat portal vein were studied. L-arginine increased the frequency of spontaneous contraction concentration-dependently between 10 microM and 1 mM. Changes in contraction amplitude and duration were not remarkable. D-arginine had a negligible effect on spontaneous contraction. N(omega)-nitro-L-arginine (1 mM) did not affect spontaneous contraction or the response to L-arginine. Addition of N(G)-monomethyl-L-arginine (1 mM), l-lysine (1 mM) or N-ethymaleimide (0.1 mM) increased the frequency of spontaneous contractions and inhibited the effect of L-arginine. Glibenclamide (10 microM) did not affect spontaneous contraction or the response to L-arginine. Spontaneous increase in concentration of intracellular Ca2+, estimated as the ratio of Fura-PE3 fluorescence occurred synchronously with spontaneous contraction. Spontaneous increase in concentration of intracellular Ca2+ occurred more frequently in the presence of L-arginine (1 mM). L-arginine (1 mM) also increased the number of action potential bursts/min in the longitudinal smooth muscle layer. L-arginine (1 mM) also depolarized cell membranes. This study indicates that L-arginine increases the frequency of spontaneous contraction of longitudinal muscle in the rat portal vein by membrane depolarization through mechanisms that do not involve nitric oxide or the inhibition of ATP-sensitive K+ channels.

“…In longitudinal muscle of portal vein, phasic mechanical activity has been shown to be associated with spike burst activity (Funaki and Bohr, 1964). We have previously reported increase in duration and spike number of spontaneous action potential, while no difference in the resting membrane potential was observed (Shimamura et al, 1989). No difference in the membrane potential has also been reported in SHR (Kuriyama and Suzuki, 1978).…”

Section: Discussionmentioning

confidence: 95%

“…In longitudinal preparation of portal vein from SHR, sensitivity to extracellular Ca2+ was reported to be increased (Harris et al, 1984) or same (Greenberg and Bohr, 1975) when compared with that of WKY. We have reported that the Ca-induced contraction in K+-depolarized preparation was greater in the preparation from stroke-prone SHR (SHRSP ; Okamoto et al, 1974) compared with that of the preparation from WKY, without change of sensitivity to extracellular Ca2+ (Shimamura et al, 1989). In permeabilized preparations of longitudinal smooth muscle of portal vein from hypertensive rats, response to intracellular Ca2+ has been shown to be increased (Soloviev and Bershtein, 1992).…”

Section: Introductionmentioning

confidence: 99%

Ca2+-Sensitivity of Portal Vein Circular Muscle from Normotensive and Hypertensive Rats.

Zou

Matsuda

et al. 1998

J. Smooth Muscle Res.

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Contractile sensitivity to Ca2+ was studied in rat portal vein circular muscle isolated from normotensive Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). There was no difference in resting membrane potential between WKY and SHRSP. Elevation of extracellular K+ concentration induced similar increase in tension in preparations from WKY and SHRSP. High K+-depolarized preparation developed tension increase when extracellular Ca2+ concentration was increased. The sensitivity to extracel lular Ca2+ was similar in preparations from WKY and SHRSP. Permeabilized preparation contracted when free Ca2+ concentration was increased. Sensitivity of permeabilized preparation to Ca2+ was similar in preparations from WKY and SHRSP. These results indicate that regulation of contraction by Ca2+ was similar between WKY and SHRSP. Since there was no change in high K-induced contraction in intact preparations or Cainduced contraction in permeabilized preparations, there seemed to be no difference in influx via voltage-dependent channels in portal vein circular muscle from WKY and SHRSP.