The nitric oxide synthesis/pathway mediates the inhibitory serotoninergic responses of the pressor effect elicited by sympathetic stimulation in diabetic pithed rats

García, Miguel Angel Sendín; Morán, Asunción; Martín, María Luisa; Barthelmebs, Mariette; Román, Luís San

doi:10.1016/j.ejphar.2006.03.020

Cited by 23 publications

(24 citation statements)

References 42 publications

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“…4). 5-HT can increase NO production from several different types of cells and tissues (Arima et al, 1996;Manivet et al, 2000;Borgdorff et al, 2002;Bellou et al, 2003;Borgdorff and Tangelder, 2006;García et al, 2006;Chanrion et al, 2007). Hoffmann et al (1990) described 5-HT receptors as mediating the long-lasting decrease in blood pressure after exercise and implicated 5-HT 1 and 5-HT 2 receptors in mediating this response.…”

Section: -Ht and Blood Pressurementioning

confidence: 99%

Serotonin and Blood Pressure Regulation

et al. 2012

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Section: -Ht and Blood Pressurementioning

confidence: 99%

Serotonin and Blood Pressure Regulation

et al. 2012

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“…Diabetes was induced in 115 animals by injection of alloxan (150 mg/kg, s.c.) [7][8][9]. The animals were maintained on tap water and regular food ad libitum for 8 weeks; age-matched animals were used as controls.…”

Section: Induction Of Diabetes and Animal Maintenancementioning

confidence: 99%

“…Our group has already demonstrated that in shortterm-diabetic animals, the NO synthesis/pathway mediates the 5-HT inhibitory action on the pressor responses elicited by electrical stimulation whereas NO is completely devoid of any action in normoglycaemic animals [8].…”

Section: Introductionmentioning

confidence: 99%

“…Our group and other authors have already reported that 5-HT modulates cardiovascular responses to sympathetic stimulation in normoglycaemic, short-term and long-term-diabetic animals [4][5][6][7][8][9][10]. Restrepo Several studies have suggested a possible role for 5-HT in the pathophysiology of diabetic complications (nervous system alterations and diabetes-related vascular complications).…”

Section: Introductionmentioning

confidence: 99%

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The Cyclooxygenase and Nitric Oxide Synthesis/Pathways Mediate the Inhibitory Serotonergic Response to the Pressor Effect Elicited by Sympathetic Stimulation in Long-Term Diabetic Pithed Rats

et al. 2012

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We investigated the mechanisms involved in the 5-hydroxytriptaminergic inhibitory action on the pressor responses elicited by sympathostimulation in long-term-diabetic pithed rats. Diabetes was induced in rats by alloxan administration. Eight weeks later, the animals were anaesthetized and pithed. The action and mechanisms of 5-HT were analysed based on the pressor responses induced by sympathostimulation. In 8-week-diabetic animals, 5-HT (20 µg/kg/min) inhibits the pressor effect of sympathostimulation which is reproduced by two selective 5-HT_1A and 5-HT₂ receptor agonists: 8-hydroxydipropylaminotetralin hydrobromide (8-OH-DPAT, 5 µg/kg/min) and α-methyl-5-HT (5 µg/kg/min). A bolus injection of 1H-[1,2,4] oxadiazolo[4,3-a] quinoxalin-1-one (ODQ, 10 µg/kg), or L-arginine HCl, N^ω-L-arginine methyl ester hydrochloride (L-NAME, 10 mg/kg), an inhibitor of NO production, prior to the infusion of 8-OH-DPAT (5 µg/kg/min) reversed the inhibitory effect of 8-OH-DPAT. The inhibitory effect of infusion of α-methyl 5-HT (5 µg/kg/min) was abolished in the presence of indomethacin (2 mg/kg), a non-selective cyclooxygenase (COX) inhibitor, or FR 122047 (1.5 mg/kg) or nimesulide (1.5 mg/kg), two selective COX-1 and COX-2 inhibitors, respectively, in long-term-diabetic pithed rats. Our results indicate that 5-HT inhibition of the pressor responses induced by electrical stimulation is mediated both by the NO and COX pathways in long-term-diabetic rats.

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“…Inhibition of NOS could result in the reduction of superoxide generation and the diminished contractile response to EFS observed in the L -NAME-incubated rat trachea. There is also the possibility of inhibition of serotonin release from prejunctional nerves by L -NAME, an effect that has been described by Garcia et al [29] for sympathetic outflow studies in pithed rats. Nonetheless, when the rat trachea was pre-incubated in L -NAME and contracted with EFS, the addition of 1 or 10 µ M Sal could not elicit a significant relaxation response (fig.…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Is Involved in the Response of the Isolated Intact and Epithelium-Denuded Rat Trachea to the β<sub>2</sub> Adrenergic Receptor Agonist Salbutamol

Montalvo

Cantres-Fonseca²,

Santos³

et al. 2010

Respiration

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Background: The involvement of the airway smooth muscle mediator nitric oxide (NO) in the actions of the β₂ agonist salbutamol (Sal), a well- known bronchodilator, is very poorly understood. Objectives: To determine if endogenous NO release is a major factor in the Sal-induced relaxation of the carbachol- and electrical field-stimulated rat trachea and determine the role of the tracheal epithelium as the possible source of NO involved in these effects. Methods: Isolated carbachol- or electric field-stimulated pre-contracted in vitro male Sprague Dawley rat tracheas (with epithelium intact or denuded) were relaxed with incremental or discrete concentrations of Sal in the presence and absence of the NO synthesis inhibitor L-NAME. Results: Epithelium-denuded tracheas showed a reduced relaxation response to Sal. L-NAME (1 mM) similarly decreased the sensitivity of the rat tracheas to Sal in both epithelium-intact and -denuded conditions. In the presence of L-NAME, high concentrations of Sal induced an unexpectedly large relaxation response in carbachol-stimulated rat tracheas with both intact and denuded epithelium. Sal relaxation was also affected by L-NAME in electrical field-stimulated epithelium-intact and -denuded tracheas. Conclusion: The results suggest that NO derived from sources other than the epithelium is an important mediator of the Sal-induced relaxation in rat tracheas.

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The nitric oxide synthesis/pathway mediates the inhibitory serotoninergic responses of the pressor effect elicited by sympathetic stimulation in diabetic pithed rats

Cited by 23 publications

References 42 publications

Serotonin and Blood Pressure Regulation

Serotonin and Blood Pressure Regulation

The Cyclooxygenase and Nitric Oxide Synthesis/Pathways Mediate the Inhibitory Serotonergic Response to the Pressor Effect Elicited by Sympathetic Stimulation in Long-Term Diabetic Pithed Rats

Nitric Oxide Is Involved in the Response of the Isolated Intact and Epithelium-Denuded Rat Trachea to the β<sub>2</sub> Adrenergic Receptor Agonist Salbutamol

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