ArticleThe Journal of physiology1998
Mechanisms of Ca2+ sensitization of force production by noradrenaline in rat mesenteric small arteries.
Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 58 citations in OpenAlex.
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- Involvement of transglutaminase 2 and voltage-gated potassium channels in cystamine vasodilatation in rat mesenteric small arteries.British journal of pharmacology · 2016Article
- Neural programming of mesenteric and renal arteries.American journal of physiology. Heart and circulatory physiology · 2014Article
- Enhancement of myofilament calcium sensitivity by acute hypoxia in rat distal pulmonary arteries.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Differential [Ca2+]i signaling of vasoconstriction in mesenteric microvessels of normal and reduced uterine perfusion pregnant rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2008Article
- Role of protein kinase C isozymes in the regulation of alpha1-adrenergic receptor-mediated contractions in ovine uterine arteries.Biology of reproduction · 2008Article
- Nonviral gene transfer to skeletal, smooth, and cardiac muscle in living animals.American journal of physiology. Cell physiology · 2005Review
- CPI-17-deficient smooth muscle of chicken.The Journal of physiology · 2004Article
- Comparison of U46619-, endothelin-1- or phenylephrine-induced changes in cellular Ca2+ profiles and Ca2+ sensitisation of constriction of pressurised rat resistance arteries.British journal of pharmacology · 2004Article
- Electroporation of the vasculature and the lung.DNA and cell biology · 2003Review
- Preservation of vascular contraction during ageing: dual effect on calcium handling and sensitization.British journal of pharmacology · 2003Article
- The role of RhoA and Rho-associated kinase in vascular smooth muscle contraction.Current hypertension reports · 2003Review
- Essential role of rho kinase in the Ca2+ sensitization of prostaglandin F(2alpha)-induced contraction of rabbit aortae.The Journal of physiology · 2003Article
- Nonviral gene transfer strategies for the vasculature.Microcirculation (New York, N.Y. : 1994) · 2002Review
- Noradrenaline-induced changes in intracellular Ca(2+) and tension in mesenteric arteries from diabetic rats.British journal of pharmacology · 2001Article
- Thiophosphorylation-induced Ca(2+) sensitization of guinea-pig ileum contractility is not mediated by Rho-associated kinase.The Journal of physiology · 2001Article
- Microtubule disruption modulates the Rho-kinase pathway in vascular smooth muscle.Journal of muscle research and cell motility · 2001Article
- The involvement of protein kinase C in myosin phosphorylation and force development in rat tail arterial smooth muscle.The Biochemical journal · 2000Article
- Inhibition of smooth-muscle myosin-light-chain phosphatase by Ruthenium Red.The Biochemical journal · 2000Article
- The involvement of intracellular Ca(2+) in 5-HT(1B/1D) receptor-mediated contraction of the rabbit isolated renal artery.British journal of pharmacology · 2000Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Mechanisms of Ca2+ sensitization of force production by noradrenaline were investigated by measuring contractile responses, intracellular Ca2+ concentration ([Ca2+]i) and phosphorylation of the myosin light chain (MLC) in intact and alpha-toxin-permeabilized rat mesenteric small arteries. 2. The effects of noradrenaline were investigated at constant membrane potential by comparing fully depolarized intact arteries in the absence and presence of noradrenaline. Contractile responses to K-PSS (125 mM K+) and NA-K-PSS (K-PSS + 10 microM noradrenaline) were titrated to 30 and 75%, respectively, of control force, by adjusting extracellular Ca2+ ([Ca2+]o). At both force levels, [Ca2+]i was substantially lower with NA-K-PSS than with K-PSS. With K-PSS, the proportion of MLC phosphorylated (approximately 30%) was similar at 30 and 75% of control force; with NA-K-PSS, MLC phosphorylation was greater at the higher force level (40 vs. 34%). 3. In alpha-toxin-permeabilized arteries, the force response to 1 microM Ca2+ was increased by 10 microM noradrenaline, and MLC phosphorylation was increased from 35 to 45%. The protein kinase C (PKC) inhibitor calphostin C (100 nM) abolished the noradrenaline-induced increase in MLC phosphorylation and contractile response, without affecting the contraction in response to Ca2+. Treatment with ATP gamma S in the presence of the MLC kinase inhibitor ML-9 increased the sensitivity to Ca2+ and abolished the response to noradrenaline. 4. The present results show that that in rat mesenteric small arteries noradrenaline-induced Ca2+ sensitization is associated with an increased proportion of phosphorylated MLC. The results are consistent with a decreased MLC phosphatase activity mediated through PKC. Furthermore, while MLC phosphorylation is a requirement for force production, the results show that other factors are also involved in force regulation.
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