Incubation of rat aortic rings produces a specific reduction in agonist-evoked contraction: effect of age of donor

Resende, Ângela Castro; Tabellion, Aurore; Nadaud, Sophie; Lartaud, Isabelle; Bagrel, Denyse; Faure, Sébastien; Atkinson, Jeffrey; Capdeville-Atkinson, Christine

doi:10.1016/j.lfs.2004.04.058

Cited by 11 publications

(27 citation statements)

References 24 publications

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“…The finding that there was no change in the response to phenylephrine in both the 2-and 24-h-cultured porcine PA compared with that observed in freshly prepared PA differs significantly from results obtained in cultured rat aorta (1,22,33). Increased iNOS expression was observed in these studies of endothelium-denuded (1,22) and endothelium-intact (33) aorta after 18 -24 h in culture.…”

Section: Discussioncontrasting

confidence: 80%

“…This preparation permits exposure of vascular smooth muscle to known concentrations of NO donor, contractile agonists, and other agents that are less easily controlled in vivo. While cultured aorta from rats with endothelium removed demonstrate increased inducible NOS (iNOS) expression (1,22,33), this is not the case for culture porcine PA (31).…”

Section: Discussionmentioning

confidence: 99%

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Prolonged NO treatment decreases α-adrenoreceptor agonist responsiveness in porcine pulmonary artery due to persistent soluble guanylyl cyclase activation

Perkins¹,

Kost²,

Danielson³

2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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A cultured porcine pulmonary artery (PA) model was used to examine the effects of prolonged nitric oxide (NO) treatment on the response of this vessel to acutely applied NO and to the alpha-adrenoreceptor agonist phenylephrine. Two-hour treatment with the NO donor (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NO) decreased both NO and phenylephrine responsiveness. Twenty-four-hour treatment with DETA-NO resulted in a further reduction in NO responsiveness but no further reduction in phenylephrine responsiveness. Acute addition of soluble guanylyl cyclase (sGC) inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) had no effect on phenylephrine responsiveness in PA not treated with DETA-NO. ODQ treatment fully restored phenylephrine responsiveness in PA treated with DETA-NO. sGCbeta(1) subunit protein levels in PA tissue homogenate were 48.6 +/- 6.9, 51.6 +/- 3.5, and 41.3 +/- 2.8 ng/mg total protein for freshly prepared and 2-h and 24-h NO-treated PA, respectively. Steady-state tissue cGMP was not significantly different in control versus NO-treated PA. sGC specific activity in the absence of added NO was measured in PA homogenate and was 0.29 +/- 0.02, 1.38 +/- 0.12, and 0.53 +/- 0.08 micromol cGMP.min(-1).mg sGC(-1), in freshly prepared and 2-h and 24-h NO treated PA, respectively. Ten-minute Hb treatment completely normalized sGC basal activity in homogenates prepared from DETA-NO-treated PA, which was 0.23 +/- 0.02, 0.18 +/- 0.03, and 0.25 +/- 0.04 micromol cGMP.min(-1).mg sGC(-1), in freshly prepared and 2-h and 24-h NO-treated PA, respectively. The kinetics of the Hb reversal of NO-mediated sGC persistent activation do not support sGC covalent modification as the activation mechanism. We conclude that prolonged NO exposure results in a persistently increased sGC specific activity, which accounts for the observed alpha-adrenoreceptor agonist hyporesponsiveness.

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Section: Discussioncontrasting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Prolonged NO treatment decreases α-adrenoreceptor agonist responsiveness in porcine pulmonary artery due to persistent soluble guanylyl cyclase activation

Perkins¹,

Kost²,

Danielson³

2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Despite the elevated metabolic rate of rat aortas, the tension (in mg·tension·mg -1 ·wet·mass) produced by KCl contraction of rat aortas, which varies from 240 ) to 720 (Resende et al, 2004) is only 2.5-7.5 times greater than a KCl contraction of hagfish dorsal aorta (94±12, N=4; data from this study). Thus is appears in rat vessels that either more oxygen is consumed for noncontractile-related activities, or that force development is energetically less efficient.…”

Section: Effect Of P O 2 On O 2 Consumptionmentioning

confidence: 49%

Oxygen dependency of hydrogen sulfide-mediated vasoconstriction in cyclostome aortas

Olson

Forgan

Dombkowski

et al. 2008

Journal of Experimental Biology

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SUMMARYHydrogen sulfide (H 2 S) has been proposed to mediate hypoxic vasoconstriction (HVC), however, other studies suggest the vasoconstrictory effect indirectly results from an oxidation product of H 2 S. Here we examined the relationship between H 2 S and O 2 in isolated hagfish and lamprey vessels that exhibit profound hypoxic vasoconstriction. In myographic studies, H 2 S (Na 2 S) dose-dependently constricted dorsal aortas (DA) and efferent branchial arteries (EBA) but did not affect ventral aortas or afferent branchial arteries; effects similar to those produced by hypoxia. Sensitivity of H 2 S-mediated contraction in hagfish and lamprey DA was enhanced by hypoxia. HVC in hagfish DA was enhanced by the H 2 S precursor cysteine and inhibited by amino-oxyacetate, an inhibitor of the H 2 S-synthesizing enzyme, cystathionine β-synthase. HVC was unaffected by propargyl glycine, an inhibitor of cystathionine λ-lyase. Oxygen consumption (M O 2) of hagfish DA was constant between 15 and 115·mmHg P O 2 (1·mmHg=0.133·kPa), decreased when P O 2 <15·mmHg, and increased after P O 2 exceeded 115·mmHg. 10·μmol·l -1 H 2 S increased and у100·μmol·l -1 H 2 S decreased M O 2. Consistent with the effects on HVC, cysteine increased and amino-oxyacetate decreased M O 2. These results show that H 2 S is a monophasic vasoconstrictor of specific cyclostome vessels and because hagfish lack vascular NO, and vascular sensitivity to H 2 S was enhanced at low P O 2, it is unlikely that H 2 S contractions are mediated by either H 2 S-NO interaction or an oxidation product of H 2 S. These experiments also provide additional support for the hypothesis that the metabolism of H 2 S is involved in oxygen sensing/signal transduction in vertebrate vascular smooth muscle.

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“…To amplify iNOS and GAPDH cDNA, sense and antisense oligonucleotide primers were designed based on the published cDNA sequences (66). Oligonucleotides were obtained from Sigma-Genosys (St. Louis, MO).…”

Section: Methodsmentioning

confidence: 99%

Impaired insulin-mediated vasorelaxation in diabetic Goto-Kakizaki rats is caused by impaired Akt phosphorylation

Lee¹,

Palaia²,

Ragolia³

2009

American Journal of Physiology-Cell Physiology

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Insulin resistance associated with Type 2 diabetes contributes to impaired vasorelaxation. Previously, we showed the phosphorylation of myosin-bound phosphatase substrate MYPT1, a marker of the vascular smooth muscle cell (VSMC) contraction, was negatively regulated by Akt (protein kinase B) phosphorylation in response to insulin stimulation. In this study we examined the role of Akt phosphorylation on impaired insulin-induced vasodilation in the Goto-Kakizaki (GK) rat model of Type 2 diabetes. GK VSMCs had impaired basal and insulin-induced Akt phosphorylation as well as increases in basal MYPT1 phosphorylation, inducible nitric oxide synthase (iNOS) expression, and nitrite/nitrate production compared with Wistar-Kyoto controls. Both iNOS expression and the inhibition of angiotensin (ANG) II-induced MYPT1 phosphorylation were resistant to the effects of insulin in diabetic GK VSMC. We also measured the isometric tension of intact and denuded GK aorta using a myograph and observed significantly impaired insulin-induced vasodilation. Adenovirus-mediated overexpression of constitutively active Akt in GK VSMC led to significantly improved insulin sensitivity in terms of counteracting ANG II-induced contractile signaling via MYPT1, myosin light chain dephosphorylation, and reduced iNOS expression, S-nitrosylation and survivin expression. We demonstrated for the first time the presence of Akt-independent iNOS expression in the GK diabetic model and that the defective insulin-induced vasodilation observed in the diabetic vasculature can be restored by the overexpression of active Akt, which advocates a novel therapeutic strategy for treating diabetes.

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Incubation of rat aortic rings produces a specific reduction in agonist-evoked contraction: effect of age of donor

Cited by 11 publications

References 24 publications

Prolonged NO treatment decreases α-adrenoreceptor agonist responsiveness in porcine pulmonary artery due to persistent soluble guanylyl cyclase activation

Prolonged NO treatment decreases α-adrenoreceptor agonist responsiveness in porcine pulmonary artery due to persistent soluble guanylyl cyclase activation

Oxygen dependency of hydrogen sulfide-mediated vasoconstriction in cyclostome aortas

Impaired insulin-mediated vasorelaxation in diabetic Goto-Kakizaki rats is caused by impaired Akt phosphorylation

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