Myoplasmic [Ca2+] determines myosin phosphorylation in agonist-stimulated swine arterial smooth muscle.

Rembold, Christopher M.; Murphy, Richard A.

doi:10.1161/01.res.63.3.593

Cited by 207 publications

(152 citation statements)

References 32 publications

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“…This suggests that a transient MLC phosphorylation is sufficient to induce a prolonged EC contraction comparable to the latchbridge state in smooth muscle cells, wherein maintenance of contraction occurs despite MLC dephosphorylation. 44 A transient MLC phosphorylation does not necessarily lead to prolonged barrier dysfunction. Histamine was shown previously 4 to induce a very similar MLC phosphorylation, but it reduced barrier function in a transient and Rhoindependent way.…”

Section: Discussionmentioning

confidence: 99%

Role of RhoA and Rho Kinase in Lysophosphatidic Acid–Induced Endothelial Barrier Dysfunction

Amerongen

Vermeer

Hinsbergh

2000

ATVB

139

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Abstract-In the present study, the roles of the small GTPase RhoA and its target Rho kinase in endothelial permeability were investigated in vitro. We have shown previously that, in addition to a rise in the intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ), RhoA is involved in the prolonged thrombin-induced barrier dysfunction. To study the role of RhoA and Rho kinase more specifically, endothelial cells were stimulated with lysophosphatidic acid (LPA), a commonly used RhoA activator. LPA induced a 2-to 3-fold increase in the passage of horseradish peroxidase (HRP) across endothelial monolayers that lasted for several hours, whereas thrombin induced a 5-to 10-fold increase. Comparable to the thrombin-induced barrier dysfunction, the LPA-induced barrier dysfunction was accompanied by a reorganization of the

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Section: Discussionmentioning

confidence: 99%

Role of RhoA and Rho Kinase in Lysophosphatidic Acid–Induced Endothelial Barrier Dysfunction

Amerongen

Vermeer

Hinsbergh

2000

ATVB

139

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“…The developed force was corrected for the cross-sectional area of each individual strip and was expressed as active stress (N/m 2 ) using the equation stress ϭ force/cross-sectional area, where cross-sectional area ϭ wet weight/(tissue density ϫ length of strip), and tissue density ϭ 1.055 g/cm 3 as previously described (35,59). Data from vascular strips of the same animal were averaged and presented as data from one animal, and n represented the number of animals.…”

Section: Animalsmentioning

confidence: 99%

TNF-α enhances contraction and inhibits endothelial NO-cGMP relaxation in systemic vessels of pregnant rats

Giardina

Green

Cockrell

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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. TNF-␣ enhances contraction and inhibits endothelial NO-cGMP relaxation in systemic vessels of pregnant rats. Am J Physiol Regulatory Integrative Comp Physiol 283: R130-R143, 2002. First published February 28, 2002 10.1152/ajpregu.00704. 2001.-Tumor necrosis factor-␣ (TNF-␣) is elevated in the plasma of preeclamptic women and may have a role in pregnancy-induced hypertension. However, whether the hemodynamic effects of TNF-␣ reflect the direct effects on vascular reactivity is unclear. We tested the hypothesis that TNF-␣ impairs endothelium-dependent relaxation and enhances vascular contraction in systemic vessels of pregnant rats. We measured isometric contraction in aortic strips isolated from virgin and pregnant Sprague-Dawley rats (nontreated vs. treated for 2 h with 10-1,000 pg/ml TNF-␣). In endotheliumintact vascular strips, TNF-␣ caused greater enhancement of phenylephrine (Phe) contraction in pregnant than virgin rats. TNF-␣ caused significant inhibition of ACh-and bradykinin-induced vascular relaxation and nitrite/nitrate production that were more prominent in pregnant than virgin rats. N G -nitro-L-arginine methyl ester [L-NAME, 100 M, an inhibitor of nitric oxide (NO) synthase] or 1H-[1,2,4]oxadiazolo[4,3]-quinoxalin-1-one (ODQ, 1 M, an inhibitor of cGMP production in smooth muscle) inhibited ACh relaxation and enhanced Phe contraction in nontreated but to a lesser extent in TNF-␣-treated vessels, particularly those of pregnant rats. Endothelium removal enhanced Phe contraction in nontreated but not TNF-␣-treated vessels, especially those of pregnant rats. Relaxation of Phe contraction with the NO donor sodium nitroprusside was not different between nontreated and TNF-␣-treated vessels. Thus TNF-␣ enhances vascular contraction and inhibits endothelium-dependent NO-cGMP-mediated vascular relaxation in systemic vessels, particularly those of pregnant rats. The results support a direct role for TNF-␣ as a possible mediator of increased vascular resistance associated with pregnancy-induced hypertension.cytokines; endothelium; nitric oxide; pregnancy; arterial pressure; tumor necrosis factor-␣ NORMAL PREGNANCY IS OFTEN associated with decreased systemic vascular resistance and arterial pressure and reduced vascular reactivity to circulating vasoconstrictors (20,35,46,51). The hemodynamic and vascular changes associated with normal pregnancy have been attributed in part to increased nitric oxide (NO) synthesis by various cells including the vascular endothelial cells (1,18,54,62,69). This is supported by studies showing that the tissue expression and activity of NO synthase (NOS) are enhanced during late gestation (4,13,61,68) and that the metabolic production and plasma level of guanosine 3Ј,5Ј-cyclic monophosphate (cGMP), a second messenger of NO and a cellular mediator of vascular smooth muscle relaxation (30,34), are increased during pregnancy (15).In 5-10% of pregnancies, women develop a condition called preeclampsia, which is characterized by proteinuria, increased intravascular coagulation and sy...

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“…It is now generally accepted that the resultant phosphorylation of the 20 kDa myosin light chain (MLC20) leads to the interaction of actin with myosin, triggering a contractile response [2]. Recent studies have shown that the [Ca2+]~ is not the sole determinant for the extent of phosphorylation of MLC20 achieved by agonist stimulation [3][4][5][6][7]. Thus, as compared to KC1 depolarization, excitatory agonist consistently produces larger increases in both MLC20 phosphorylation and tension at a given level of the [Ca2+]~, implying that agonists somehow enhance the Ca 2+ sensitivity of both MLC20 phosphorylation and contraction [3,4,6].…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies have shown that the [Ca2+]~ is not the sole determinant for the extent of phosphorylation of MLC20 achieved by agonist stimulation [3][4][5][6][7]. Thus, as compared to KC1 depolarization, excitatory agonist consistently produces larger increases in both MLC20 phosphorylation and tension at a given level of the [Ca2+]~, implying that agonists somehow enhance the Ca 2+ sensitivity of both MLC20 phosphorylation and contraction [3,4,6]. Indeed, it has recently been demonstrated in skinned smooth muscle fibers that, at a fixed level of [Ca2+]i, an agonist causes increases in the phosphorylation level of MLC20 and tension in a GTP-dependent manner, providing evidence for the involvement of a GTP binding protein (G protein) in receptor-mediated sensitization of Ca 2+-dependent MLC20 phosphorylation [5,7,8].…”

Section: Introductionmentioning

confidence: 99%

Involvement of rho in GTPγS‐induced enhancement of phosphorylation of 20 kDa myosin light chain in vascular smooth muscle cells: inhibition of phosphatase activity

et al. 1995

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In ~-escin-permeabilized cultured pig aortic smooth muscle cells GTP2/S dose-dependently enhances Ca2÷-induced, wortmannin-sensitive phosphorylation of 20 kDa myosin light chain (MLC~o). GTP~S does not potentiate thiophosphorylation of MLCzo, but does inhibit its dephosphorylation. Pretreatment with C. botulinum exotoxin C3, which specifically ADP-ribosylates and inactivates the rho family of the small molecular weight G proteins, completely abolishes the effects of GTPyS. These results indicate that rho is involved in the GTP?/S-induced enhancement of Ca2+-dependent MLC20 phosphorylation in aortic smooth muscle cells, and strongly suggest that this effect of rho is due to inhibition of protein phosphatase activity toward MLC2o.

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Myoplasmic [Ca2+] determines myosin phosphorylation in agonist-stimulated swine arterial smooth muscle.

Cited by 207 publications

References 32 publications

Role of RhoA and Rho Kinase in Lysophosphatidic Acid–Induced Endothelial Barrier Dysfunction

Role of RhoA and Rho Kinase in Lysophosphatidic Acid–Induced Endothelial Barrier Dysfunction

TNF-α enhances contraction and inhibits endothelial NO-cGMP relaxation in systemic vessels of pregnant rats

Involvement of rho in GTPγS‐induced enhancement of phosphorylation of 20 kDa myosin light chain in vascular smooth muscle cells: inhibition of phosphatase activity

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