Noradrenaline stimulation of high-affinity GTPase activity in membranes from rat aorta and caudal artery

Weber, Lynn P.; MacLeod, Kathleen M.

doi:10.1016/0006-2952(96)00344-9

Cited by 6 publications

(2 citation statements)

References 27 publications

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“…A requirement for GTP to maintain Ca 2+ sensitivity in the absence of noradrenaline has also been noted previously (Akata, 1996). It was of interest that the concentration of GTP required (2 μM) was similar to the K m value reported for the high affinity GTPase activity of GTP‐binding proteins in caudal artery membranes (in the range from 0.24 to 1 μM, Weber & MacLeod, 1996). The concentration of GTP required was, however, two orders of magnitude less than the concentrations of free GTP which have been reported in smooth muscle (Coburn, Azim, Fillers & Baron, 1993), and it is therefore unlikely, as was pointed out by these authors, that changing levels of GTP in vivo could be a limiting or regulatory factor for contraction.…”

Section: Discussionsupporting

confidence: 67%

Mechanisms of Ca²⁺ sensitization of force production by noradrenaline in rat mesenteric small arteries

Buus

Aalkjær

Nilsson

et al. 1998

The Journal of Physiology

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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 α‐toxin‐permeabilized rat mesenteric small arteries. 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 μM 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 (≈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 %). In α‐toxin‐permeabilized arteries, the force response to 1 μM Ca2+ was increased by 10 μM 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 ATPγS in the presence of the MLC kinase inhibitor ML‐9 increased the sensitivity to Ca2+ and abolished the response to noradrenaline. The present results show 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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Section: Discussionsupporting

confidence: 67%

Mechanisms of Ca²⁺ sensitization of force production by noradrenaline in rat mesenteric small arteries

Buus

Aalkjær

Nilsson

et al. 1998

The Journal of Physiology

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“…It has previously been showed that aadrenoceptors and especially a 1 -adrenoceptors, can couple to multiple transduction pathways (Orowio et al, 1992;GarciaSainz, 1993) including G i -protein-mediated pathways (Fujiwara et al, 1989;Aburto et al, 1993;D'Angelo & Osol, 1994). PTX-sensitive G i -proteins have been isolated from the rat tail artery smooth muscle cell (Weber & MacLeod, 1996;Petitcolin et al, 1998). The present results show that in the de-endothelialized rat tail artery, PTX ADP-ribosylates G iproteins.…”

Section: Discussionmentioning

confidence: 99%

Pertussis toxin‐sensitive G_i‐proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery

Spitzbarth-Régrigny¹,

Petitcolin

Bueb

et al. 2000

British J Pharmacology

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1 We studied the involvement of pertussis toxin (PTX)-sensitive G-proteins in the sensitivity of arterial constriction to intracellular calcium ([Ca 2+ ] i ) mobilization. 2 Vasoconstriction was measured in vitro in perfused, de-endothelialized rat tail arteries loaed with the calcium-sensitive dye, fura-2 and treated or not with PTX (30 ± 1000 ng ml 71 ). Arteries were stimulated with noradrenaline (NA, 0.1 ± 100 mM) or KCl (15 ± 120 mM). 3 KCl elicited a smaller vasoconstrictor response (E max =94+8 mmHg) than NA (E max =198+9 mmHg) although [Ca 2+ ] i mobilization was similar (E max =123+8 and 135+7 nM for KCl and NA, respectively). PTX (1000 ng ml 71 ) had no e ect on [Ca 2+ ] i mobilization but lowered NA-(but not KCl-) induced vasoconstriction (E max =118+7 mmHg). 4 G i/o -proteins were revealed by immunoblotting with anti-G ia and anti-G oa antibodies in membranes prepared from de-endothelialized tail arteries. [a 32 P]-ADP-ribosylation of G-proteins by PTX (1000 ng ml 71 ) was demonstrated in the intact rat tail artery (pixels in the absence of PTX: 3150, presence: 25053). 5 In conclusion, we suggest that smooth muscle cells possess a PTX-sensitive G i -protein-mediated intracellular pathway which ampli®es [Ca 2+ ] i sensitivity of contraction in the presence of agonists such as NA.

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Lack of involvement of pertussis toxin-sensitive G-proteins in norepinephrine-induced vasoconstriction of rat aorta smooth muscle11Abbreviations: α-AR, α-adrenoceptor; DTT, dl-dithiothreitol; NE, norepinephrine; PSS, physiological salt solution; PTX, pertussis-toxin; and SMC, smooth muscle cells.

Petitcolin

Vandeputte²,

Spitzbarth-Régrigny³

et al. 2001

Biochemical Pharmacology

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Noradrenaline stimulation of high-affinity GTPase activity in membranes from rat aorta and caudal artery

Cited by 6 publications

References 27 publications

Mechanisms of Ca²⁺ sensitization of force production by noradrenaline in rat mesenteric small arteries

Mechanisms of Ca²⁺ sensitization of force production by noradrenaline in rat mesenteric small arteries

Pertussis toxin‐sensitive G_i‐proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery

Lack of involvement of pertussis toxin-sensitive G-proteins in norepinephrine-induced vasoconstriction of rat aorta smooth muscle11Abbreviations: α-AR, α-adrenoceptor; DTT, dl-dithiothreitol; NE, norepinephrine; PSS, physiological salt solution; PTX, pertussis-toxin; and SMC, smooth muscle cells.

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Noradrenaline stimulation of high-affinity GTPase activity in membranes from rat aorta and caudal artery

Cited by 6 publications

References 27 publications

Mechanisms of Ca2+ sensitization of force production by noradrenaline in rat mesenteric small arteries

Mechanisms of Ca2+ sensitization of force production by noradrenaline in rat mesenteric small arteries

Pertussis toxin‐sensitive Gi‐proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery

Lack of involvement of pertussis toxin-sensitive G-proteins in norepinephrine-induced vasoconstriction of rat aorta smooth muscle11Abbreviations: α-AR, α-adrenoceptor; DTT, dl-dithiothreitol; NE, norepinephrine; PSS, physiological salt solution; PTX, pertussis-toxin; and SMC, smooth muscle cells.

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Mechanisms of Ca²⁺ sensitization of force production by noradrenaline in rat mesenteric small arteries

Mechanisms of Ca²⁺ sensitization of force production by noradrenaline in rat mesenteric small arteries

Pertussis toxin‐sensitive G_i‐proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery