Arterial endothelium-derived relaxing factor (AEDRF) does not suppress papillary muscle or portal vein contractions

Vedernikov, Yuri P.; Vihert, A. M.; Leisner, H

doi:10.1016/0014-2999(87)90091-4

Cited by 9 publications

(4 citation statements)

References 7 publications

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“…3). Thus our observation may support previous studies (Feletou et al, 1989;Vedernikov et al, 1987) which showed negative evidence for acetylcholine-mediated EDRF in the rat portal vein. Tonic contractions induced by clonidine were endothelium-dependent (Fig.…”

Section: Discussionsupporting

confidence: 93%

“…In both longitudinal and circular muscle preparations of the hepatic portal vein, NO was shown to inhibit contraction, suggesting that contractility of the hepatic portal vein was regulated by NO (Feletou et al, 1989;Shimamura et al, 2000). However, acetylcholine-induced EDRF released from either aorta or femoral artery failed to change the spontaneous contraction of the rat portal vein longitudinal muscle preparation (Vedernikov et al, 1987;Feletou et al, 1989). Thus, the possible contributions of both EDRF and other factors released from the endothelium on the smooth muscle of the hepatic portal vein were still obscure.…”

Section: Discussionmentioning

confidence: 99%

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Clonidine induced endothelium-dependent tonic contraction in circular muscle of the rat hepatic portal vein

Shimamura

Toba

Kimura

et al. 2006

J Smooth Muscle Res

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Clonidine, an α2-agonist, has been shown to be useful in the treatment of hepatic portal hypertension in cirrhosis. The mechanism has been attributed to a clonidineinduced decrease in sympathetic activity. While clonidine has been shown to stimulate the α2-adrenoceptors of blood vessels, there is limited knowledge of the effects of clonidine on the circular muscle of the hepatic portal vein which regulates its blood flow. To investigate clonidine-induced contraction of the circular muscle of the hepatic portal vein and to clarify the possible role of the endothelium in the contraction, we examined the effects of clonidine on the isometric contraction of endothelium-intact and -removed ring preparations of the rat hepatic portal vein. In endothelium-intact preparations, clonidine caused a concentration-dependent increase in the amplitude of contractions. Inhibition of NO synthesis with N ω -nitro-L-arginine (L-NNA) elevated the resting tone, and increased the amplitude of the clonidine-induced contractions. Inhibition of cyclooxygenase by diclofenac did not change the amplitude of the clonidine-induced contractions observed both in the presence and absence of L-NNA. Application of a single concentration of clonidine induced a clear increase in amplitude of both twitch and tonic contractions. Twitch and tonic contractions induced by clonidine were inhibited by yohimbine. When the endothelium was damaged by sodium deoxycholate, tonic contractions induced by clonidine were completely suppressed, whereas the increase in twitch contractions was not influenced by chemical damage of the endothelium. Neither SKF-96365, a nonselective cation channel blocker, nor superoxide dismutase, a free radical scavenger, in the presence of catalase, changed the tonic contraction induced by clonidine. These results indicate that stimulation of α2-adrenoceptors enhanced twitch contractions and induced tonic contractions in the circular muscle of the rat hepatic portal vein, especially in the absence of NO. The latter, but not the former, occurs through an endothelium-dependent pathway.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Clonidine induced endothelium-dependent tonic contraction in circular muscle of the rat hepatic portal vein

Shimamura

Toba

Kimura

et al. 2006

J Smooth Muscle Res

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“…The experimental set-up used was similar to that described in an earlier work (15) except that one additional channel for direct physiological salt solution (PSS) was introduced (14,16). A segment of donor vessel (approximately 4 cm in length) was perfused intraluminally (channel III) and externally (channel If) (Fig.…”

Section: Bioassay Experimentsmentioning

confidence: 99%

“…Recently a suggestion concerning the identity of EDRF and nitric oxide (NO) was made (5,9). However the data appeared in the absence of venous (2,14,16), or non-vessel (11) smooth muscle relaxation under the influence of arterial EDRF, though they relaxed through nitric compound sodium-nitroprusside (2). These facts throw a shadow on the identity of NO and EDRF.…”

Section: Introductionmentioning

confidence: 96%

Heterogeneity of the response of venous smooth muscle to arterial endothelium-derived relaxing factor (EDRF) in respect of the role of nitric oxide

Vedernikov¹,

Gräser

Tiedt

et al. 1988

Basic Res Cardiol

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In bioassay and organ bath experiments, the responses of different canine venous preparations to arterial and their own EDRF were studied. Vena jugularis, vena femoralis and vena mesenterica relaxed on both EDRFs released by acetylcholine. Vena saphena, venae cordis and vena portae did not show endothelium-dependent dilation, either under bioassay or in organ bath experiments. All the veins tested relaxed completely after sodium nitroprusside administration. The identity of EDRF and nitric oxide is not confirmed by this study.

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

Shimamura

Zou²,

Matsuda³

et al. 2000

Pflugers Arch - Eur J Physiol

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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.

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Arterial endothelium-derived relaxing factor (AEDRF) does not suppress papillary muscle or portal vein contractions

Cited by 9 publications

References 7 publications

Clonidine induced endothelium-dependent tonic contraction in circular muscle of the rat hepatic portal vein

Clonidine induced endothelium-dependent tonic contraction in circular muscle of the rat hepatic portal vein

Heterogeneity of the response of venous smooth muscle to arterial endothelium-derived relaxing factor (EDRF) in respect of the role of nitric oxide

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

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