Effect of arginine analogues on rat hind paw oedema and mast cell activation in vitro

Giraldelo, Cleria M.M.; Zappellini, A.; Muscará, Marcelo Nícolas; Luca, Iara Maria Silva De; Hyslop, Stephen; Cirino, Giuseppe; Zatz, Roberto; Nucci, Gilberto De; Antunes, Edson

doi:10.1016/0014-2999(94)90698-x

Cited by 37 publications

(24 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Remembering that administration of drugs with the ability to inhibit NO production leads to a vasoconstriction, it is possible that a higher dose of L-NAME induced systemic vasoconstriction, thus preventing vascular leakage induced by inflammatory mediators released after Tsv administration. Such dual effects of L-NAME were also obtained by Giraldelo et al [30] when different doses of L-NAME were employed to pretreated rats in which bradykinin was used to induce hind paw edema. The inhibition of hind paw rat edema was also achieved by pretreatment with L-NAME when the stimuli was carregeenin or dextran [31].…”

Section: Discussionmentioning

confidence: 71%

Edematogenic Activity of Scorpion Venoms from the Buthidae Family and the Role of Platelet-Activating Factor and Nitric Oxide in Paw Edema Induced by Tityus Venoms

et al. 2008

View full text Add to dashboard Cite

We compared the edematogenic activity of venoms of scorpions from the Buthidae family, Tityus bahiensis (Tbv), Tityus serrulatus (Tsv) and Rhopalurus rochai (Rrv). Three doses (20, 40 and 80 microg/kg sc) of each venom were administrated in hind paw of mice and edema was measured from 5 min to 24 h. Tbv and Tsv both induced edema of rapid onset (135% of increase at 15 min); Rrv induced only a mild edema (40% of increase). We then investigated the involvement of platelet-activating factor (PAF) and endogenous nitric oxide (NO) in Tbv and Tsv-induced paw edema. Pretreatment of mice with a PAF antagonist (WEB-2170) inhibited Tsv but not Tbv-induced edema. Pretreatment with a non selective inhibitor of NO-synthases (L: -NAME) inhibited or increased the edema depending on the dose and the time the edema was measured. In conclusion, the venoms from Tityus are stronger inducers of edema than the venom from the Rhopalurus scorpion. The venoms of Tityus species are similar in potency and time-course edema development. PAF is involved in the edema induced only by Tsv.

show abstract

Section: Discussionmentioning

confidence: 71%

Edematogenic Activity of Scorpion Venoms from the Buthidae Family and the Role of Platelet-Activating Factor and Nitric Oxide in Paw Edema Induced by Tityus Venoms

et al. 2008

View full text Add to dashboard Cite

show abstract

“…A previous study demonstrated that, besides serving as a substrate for NOS, L-Arg can also stimulate the release of insulin and histamine to induce vasodilation (11,13,36). Meanwhile, it has been shown that insulin can induce eNOS phosphorylation at Ser 1179 and HSP90 associated with eNOS (45).…”

Section: Discussionmentioning

confidence: 99%

l-Arginine restores endothelial nitric oxide synthase-coupled activity and attenuates monocrotaline-induced pulmonary artery hypertension in rats

Wei

Huang

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

Ou JS. L-Arginine restores endothelial nitric oxide synthase-coupled activity and attenuates monocrotaline-induced pulmonary artery hypertension in rats. Am J Physiol Endocrinol Metab 298: E1131-E1139, 2010. First published March 9, 2010; doi:10.1152/ajpendo.00107.2010.-L-Arginine can attenuate pulmonary hypertension (PH) by a mechanism that are not fully understood. This study investigated the molecule mechanism of L-arginine attenuating PH. Sprague Dawley rats were treated with monocrotaline (MCT) with or without L-arginine for 3 or 5 wk. Right ventricular systolic pressure (RVSP), right heart hypertrophy, survival rate, pulmonary artery wall thickness, nitric oxide (NO) concentration, and superoxide anion (O2 ·Ϫ ) generation in the lung were measured. Expressions of endothelial nitric oxide synthase (eNOS) and heat shock protein 90 (HSP90), phosphorylation of eNOS at Ser 1177 , and the association of eNOS and HSP90 in the lung were determined by Western blot and immunoprecipitation experiments. MCT increased RVSP, right heart hypertrophy, mortality, pulmonary artery wall thickness, and O2 ·Ϫ generation and decreased eNOS and HSP90 expression and association, phosphorylation of eNOS at Ser 1177 , and NO production. L-Arginine decreased RVSP, right heart hypertrophy, mortality, O2 ·Ϫ generation, and pulmonary artery wall thickness and increased NO production. L-Arginine increased eNOS expression, phosphorylation of eNOS at Ser 1177 , and association of eNOS and HSP90 without significantly altering HSP90 expression. L-Arginine may act through three pathways, providing a substrate for NO generation, preserving eNOS expression/phosphorylation, and maintaining the association of eNOS and HSP90, which allows restoration of eNOS activity and coupling activity, to maintain the balance between NO and O2 ·Ϫ and delay the development of PH.heat shock protein 90; nitric oxide; superoxide anion THERE ARE STILL NO EFFICIENT preventive and therapeutic methods available for pulmonary hypertension (PH) due to the fact that mechanisms, especially the molecular mechanisms of PH, are still not fully understood. Endothelial nitric oxide synthase (eNOS) expression and nitric oxide (NO) production decreases in PH (10,12,14). Daily treatment with an NO donor attenuates monocrotaline (MCT)-induced PH and pulmonary vascular remodeling (23). Furthermore, supplementation with the NO precursor L-arginine (L-Arg) enhances NOS expression within the pulmonary endothelium coincident with elevated NO, increases the plasma level of L-citrulline, and reduces mean pulmonary arterial pressure, pulmonary vascular resistance, and PH mortality in patients and in animal models (4, 5, 8, 26 -29, 38, 46). However, the molecular mechanisms by which L-Arg attenuates PH remain unclear. Previous studies conducted in different animal models demonstrated that L-Arg reduces generation of superoxide anion (O 2 ·Ϫ ) and prevents the reduced expression of eNOS (40, 46). The balance between NO and O 2 ·Ϫ plays an important role in the process of many cardiovascul...

show abstract

“…L-Arginine increases insulin secretion, 26 which itself promotes vasodilation. In addition, L-arginine stimulates histamine release from mast cells, 27 which also evokes a vasodilator response. Administered as the hydrochloric acid salt, L-arginine induces an extracellular acidosis that in turn can transiently alter intracellular pH and thereby affect pH-dependent cell-signaling pathways, including calcium transients, that modulate eNOS activity and NO synthesis.…”

Section: See P 2160mentioning

confidence: 99%

What We Know and Don’t Know About l -Arginine and NO

Loscalzo

2000

Circulation

View full text Add to dashboard Cite

Effect of arginine analogues on rat hind paw oedema and mast cell activation in vitro

Cited by 37 publications

References 29 publications

Edematogenic Activity of Scorpion Venoms from the Buthidae Family and the Role of Platelet-Activating Factor and Nitric Oxide in Paw Edema Induced by Tityus Venoms

Edematogenic Activity of Scorpion Venoms from the Buthidae Family and the Role of Platelet-Activating Factor and Nitric Oxide in Paw Edema Induced by Tityus Venoms

l-Arginine restores endothelial nitric oxide synthase-coupled activity and attenuates monocrotaline-induced pulmonary artery hypertension in rats

What We Know and Don’t Know About l -Arginine and NO

Contact Info

Product

Resources

About