Alterations in cytoplasmic calcium sensitivity during porcine coronary artery contractions as detected by aequorin.

Bradley, Arlene B.; Morgan, Kathleen G.

doi:10.1113/jphysiol.1987.sp016500

Cited by 163 publications

(91 citation statements)

References 19 publications

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“…In particular, the relative density of a-and fladrenoceptors and the general pharmacological profile of porcine epicardial coronary arteries are very similar to their human counterparts (Ginsburg et al, 1980;Ginsburg, 1983;Moreland & Bohr, 1984;Bradley & Morgan, 1987). Therefore, it is probably not coincidental that the only animal model of coronary hyperreactivity and vasospasm has been developed in swine (Shimokawa et al, 1983;Egashira et al, 1986;Yamamoto et al, 1987;Isner & Chokshi, 1991).…”

Section: Systemic Haemodynamicsmentioning

confidence: 99%

Cocaine‐induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine

Lin¹,

Núñez²,

Susulic³

et al. 1996

British J Pharmacology

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Section: Systemic Haemodynamicsmentioning

confidence: 99%

Cocaine‐induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine

Lin¹,

Núñez²,

Susulic³

et al. 1996

British J Pharmacology

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“…For the measurement of relaxation, the arteries were precontracted with phenylephrine (PHE) at a concentration corresponding to the EC80 (0.3 ,UM for the preparations with (Bradley & Morgan, 1987), prostaglandin F2, (PGF2,) induced an attenuated, but sustained tonic contraction. In addition, a larger maximum contraction was produced by PGF21 than by PHE.…”

Section: Organ Bath Experimentsmentioning

confidence: 99%

Relaxation of rat thoracic aorta induced by the Ca²⁺‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation

Moritoki

Hisayama

Takeuchi

et al. 1994

British J Pharmacology

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1 The effect of the Ca2+-ATPase inhibitor, cyclopiazonic acid (CPA), was studied on rat thoracic aortic ring preparations. 2 At concentrations above 0.3 JM, CPA induced relaxation in the arteries precontracted with phenylephrine. Removal of the endothelium abolished CPA-induced relaxation.3 The nitric oxide (NO) synthase inhibitor NG-nitro L-arginine (3-300 AM), the free radical scavenger haemoglobin (O.1-33 AM), the soluble guanylate cyclase inhibitor, LY83583 (0.1-10 JAM), each inhibited the endothelium-dependent relaxation to CPA. The potassium channel blocker, glibenclamide (1O AM) and cyclo-oxygenase inhibitor, indomethacin (100 JAM for 60 min and then washed out) did not alter the action of CPA. 4 The calmodulin inhibitors calmidazolium (3-10 IAM) and W-7 (100 AM) also abolished CPA-induced relaxation.5 CPA (10 AM) increased guanosine 3':5'-cyclic monophosphate (cyclic GMP) levels in arteries with an intact endothelium, without affecting adenosine 3':5'-cyclic monophosphate (cyclic AMP) levels. 6 The inhibitors of NO synthesis and actions, the calmodulin inhibitor and removal of the endothelium abolished the CPA-stimulated increase in the levels of cyclic GMP. 7 In Ca2'-free solution, CPA failed to induce relaxation or to stimulate cyclic GMP production.Relaxation to nitroprusside was not affected under these conditions.

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“…However, as the use of Ca 2ϩ indicator revealed that the force/ Ca 2ϩ ratio is variable, the Ca 2ϩ -CaM-dependent MLC kinase pathway cannot solely account for the mechanisms of agonistor GTP␥S-induced increases in the force/Ca 2ϩ ratio, so-called Ca 2ϩ sensitization (1,(5)(6)(7)(8)(9). Thus, an additional mechanism that can regulate Ca 2ϩ sensitization of smooth muscle has been proposed.…”

mentioning

confidence: 99%

“…Using membrane permeabilization of smooth muscle, the possibility that monomeric Ras family G-proteins, such as Rho, contribute to Ca 2ϩ sensitization of smooth muscle was demonstrated (10 -12). Direct activation of G-proteins by the application of GTP␥S (8,9), agonists (1,(5)(6)(7)(8), and GTP-activated Rho (10 -12) could exert Ca 2ϩ -sensitizing effects on saponin-or ␤-escin-permeabilized smooth muscle. However, the activated Rho failed to induce Ca 2ϩ sensitization of extensively Triton X-100-permeabilized smooth muscle (11).…”

mentioning

confidence: 99%

Rho-associated Kinase Directly Induces Smooth Muscle Contraction through Myosin Light Chain Phosphorylation

Kureishi

Kobayashi

Amano

et al. 1997

Journal of Biological Chemistry

539

427

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Small GTPase Rho plays pivotal roles in the Ca 2؉ sensitization of smooth muscle. However, the GTP-bound active form of Rho failed to exert Ca 2؉ -sensitizing effects in extensively Triton X-100-permeabilized smooth muscle preparations, due to the loss of the important diffusible cofactor (Gong, M. C., Iizuka, K., Nixon, G., Browne, J. P., Hall, A., Eccleston, J. F., Sugai, M., Kobayashi, S., Somlyo, A. V., and Somlyo, A. P. (1996) Proc. Natl. Acad. Sci. U. S. A. 93, 1340 -1345). Here we demonstrate the contractile effects of Rho-associated kinase (Rho-kinase), recently identified as a putative target of Rho, on the Triton X-100-permeabilized smooth muscle of rabbit portal vein. Introduction of the constitutively active form of Rho-kinase into the cytosol of Triton X-100-permeabilized smooth muscle provoked a contraction and a proportional increase in levels of monophosphorylation of myosin light chain in both the presence and the absence of cytosolic Ca 2؉ . These effects of constitutively active Rho-kinase were wortmannin (a potent myosin light chain kinase inhibitor)-insensitive. Immunoblot analysis revealed that the amount of native Rho-kinase was markedly lower in Triton X-100-permeabilized tissue than in intact tissue. Our results demonstrate that Rho-kinase directly modulates smooth muscle contraction through myosin light chain phosphorylation, independently of the Ca 2؉ -calmodulin-dependent myosin light chain kinase pathway.Smooth muscle contraction is primarily regulated by the levels of phosphorylation of myosin light chain (MLC), 1 which has heretofore been considered to be governed by a Ca 2ϩ -calmodulin (CaM)-dependent MLC kinase pathway (1-4). However, as the use of Ca 2ϩ indicator revealed that the force/ Ca 2ϩ ratio is variable, the Ca 2ϩ -CaM-dependent MLC kinase pathway cannot solely account for the mechanisms of agonistor GTP␥S-induced increases in the force/Ca 2ϩ ratio, so-called Ca 2ϩ sensitization (1,(5)(6)(7)(8)(9). Thus, an additional mechanism that can regulate Ca 2ϩ sensitization of smooth muscle has been proposed. Using membrane permeabilization of smooth muscle, the possibility that monomeric Ras family G-proteins, such as Rho, contribute to Ca 2ϩ sensitization of smooth muscle was demonstrated (10 -12). Direct activation of G-proteins by the application of GTP␥S (8, 9), agonists (1,(5)(6)(7)(8), and GTP-activated Rho (10 -12) could exert Ca 2ϩ -sensitizing effects on saponin-or ␤-escin-permeabilized smooth muscle. However, the activated Rho failed to induce Ca 2ϩ sensitization of extensively Triton X-100-permeabilized smooth muscle (11). Considering that extensive Triton X-100-permeabilization allows higher molecular weight compounds to diffuse from the cytosol of smooth muscle of the rabbit portal vein (13), important diffusible factor(s) for the Ca 2ϩ sensitization of smooth muscle might be lost during extensive permeabilization by Triton X-100, an event that would result in no response to activated Rho.We have recently reported that Rho-kinase, which is activated by GTP-bound act...

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Alterations in cytoplasmic calcium sensitivity during porcine coronary artery contractions as detected by aequorin.

Cited by 163 publications

References 19 publications

Cocaine‐induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine

Cocaine‐induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine

Relaxation of rat thoracic aorta induced by the Ca²⁺‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation

Rho-associated Kinase Directly Induces Smooth Muscle Contraction through Myosin Light Chain Phosphorylation

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Alterations in cytoplasmic calcium sensitivity during porcine coronary artery contractions as detected by aequorin.

Cited by 163 publications

References 19 publications

Cocaine‐induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine

Cocaine‐induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine

Relaxation of rat thoracic aorta induced by the Ca2+‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation

Rho-associated Kinase Directly Induces Smooth Muscle Contraction through Myosin Light Chain Phosphorylation

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Relaxation of rat thoracic aorta induced by the Ca²⁺‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation