Chronic HgCl2 treatment increases vasoconstriction induced by electrical field stimulation: role of adrenergic and nitrergic innervation

2011 ◽  
Vol 121 (8) ◽  
pp. 331-341 ◽  
Author(s):  
Javier Blanco-Rivero ◽  
Lorena B. Furieri ◽  
Dalton V. Vassallo ◽  
Mercedes Salaices ◽  
Gloria Balfagón
Keyword(s):  
Electrical Field Stimulation ◽  
Treated Group ◽  
Field Stimulation ◽  
Electrical Field ◽  
No Donor ◽  
Low Concentrations ◽  
Vasoconstrictor Response ◽  
Rat Mesenteric Artery ◽  
Na Release

In the present study, we have investigated the possible changes in rat mesenteric artery vascular innervation function caused by chronic exposure to low doses of HgCl2 (mercuric chloride), as well as the mechanisms involved. Rats were divided into two groups: (i) control, and (ii) HgCl2-treated rats (30 days; first dose, 4.6 μg/kg of body weight; subsequent dose, 0.07 μg·kg−1 of body weight·day−1, intramuscularly). Vasomotor response to EFS (electrical field stimulation), NA (noradrenaline) and the NO donor DEA-NO (diethylamine NONOate) were studied, nNOS (neuronal NO synthase) and phospho-nNOS protein expression were analysed, and NO, O2− (superoxide anion) and NA release were also determined. EFS-induced contraction was higher in the HgCl2-treated group. Phentolamine (1 μmol/l) decreased the response to EFS to a greater extent in HgCl2-treated rats. HgCl2 treatment increased vasoconstrictor response to exogenous NA and NA release. L-NAME (NG-nitro-L-arginine methyl ester; 0.1 mmol/l) increased the response to EFS in both experimental groups, but the increase was greater in segments from control animals. HgCl2 treatment decreased NO release and increased O2− production. Vasodilator response to DEA-NO was lower in HgCl2-treated animals. Tempol increased DEA-NO-induced relaxation to a greater extent in HgCl2-treated animals. nNOS expression was similar in arteries from both experimental groups, whereas phospho-nNOS was decreased in segments from HgCl2-treated animals. HgCl2 treatment increased vasoconstrictor response to EFS as a result of, in part, reduced NO bioavailability and increased adrenergic function. These findings offer further evidence that mercury, even at low concentrations, is an environmental risk factor for cardiovascular disease.

Release of epithelium-derived PGE2 from canine trachea after antigen inhalation

1998 ◽  
Vol 274 (2) ◽  
pp. L220-L225 ◽  
Author(s):  
I. McGrogan ◽  
L. J. Janssen ◽  
J. Wattie ◽  
P. M. O’Byrne ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Electrical Field Stimulation ◽  
Tracheal Smooth Muscle ◽  
Organ Bath ◽  
Field Stimulation ◽  
Electrical Field ◽  
Concentration Response Curve

To investigate the role of prostaglandin (PG) E2 in allergen-induced hyperresponsiveness, dogs inhaled either the allergen Ascaris suum or vehicle (Sham). Twenty-four hours after inhalation, some animals exposed to allergen demonstrated an increased responsiveness to acetylcholine challenge in vivo (Hyp-Resp), whereas others did not (Non-Resp). Strips of tracheal smooth muscle, either epithelium intact or epithelium denuded, were suspended on stimulating electrodes, and a concentration-response curve to carbachol (10−9 to 10−5 M) was generated. Tissues received electrical field stimulation, and organ bath fluid was collected to determine PGE2content. With the epithelium present, all three groups contracted similarly to 10−5 M carbachol, whereas epithelium-denuded tissues from animals that inhaled allergen contracted more than tissues from Sham dogs. In response to electrical field stimulation, Hyp-Resp tissues contracted less than Sham tissues in the presence of epithelium and more than Sham tissues in the absence of epithelium. PGE2release in the muscle bath was greater in Non-Resp tissues than in Sham or Hyp-Resp tissues when the epithelium was present. Removal of the epithelium greatly inhibited PGE2release. We conclude that tracheal smooth muscle is hyperresponsive in vitro after in vivo allergen exposure only when the modulatory effect of the epithelium, largely through PGE2 release, is removed.

scholarly journals Role of cAMP and neuronal K+channels on α2-AR-induced inhibition of ACh release in equine trachea

1998 ◽  
Vol 274 (5) ◽  
pp. L827-L832
Author(s):  
Xiang-Yang Zhang ◽  
Feng-Xia Zhu ◽  
N. Edward Robinson
Keyword(s):  
Electrical Field Stimulation ◽  
Intracellular Camp ◽  
Field Stimulation ◽  
Ach Release ◽  
Electrical Field ◽  
K Channels ◽  
Parasympathetic Nerves ◽  
Pathway Activation ◽  
Before And After

To investigate the effects of changes in intracellular cAMP on α2-adrenoceptor (AR)-induced inhibition of airway acetylcholine (ACh) release, we examined the effects of the α2-AR agonist clonidine on electrical field stimulation-evoked ACh release from equine tracheal parasympathetic nerves before and after treatment with 8-bromo-cAMP or forskolin. We also tested whether charybdotoxin (ChTX)- or iberiotoxin (IBTX)-sensitive Ca2+-activated K+ channels mediate α2-AR-induced inhibition by examining the effect of clonidine in the absence and presence of ChTX or IBTX on ACh release. The amount of released ACh was measured by HPLC coupled with electrochemical detection. Clonidine (10−7 to 10−5 M) dose dependently inhibited ACh release before and after treatment with 8-bromo-cAMP (10−3 M) or forskolin (3 × 10−5M). ChTX and IBTX, both at the concentration of 5 × 10−7 M, significantly increased ACh release; however, they did not alter the magnitude of clonidine-induced inhibition. These results indicated that in equine tracheal parasympathetic nerves, α2-AR-induced inhibition of ACh release is via an intracellular cAMP-independent pathway. Activation of both ChTX- and IBTX-sensitive Ca2+-activated K+ channels inhibits the electrical field stimulation-evoked ACh release, but these channels are not involved in the α2-AR-induced inhibition of ACh release.

scholarly journals Orchidectomy increases the formation of non-endothelial thromboxane A2 and modulates its role in the electrical field stimulation-induced response in rat mesenteric artery

2008 ◽  
Vol 197 (2) ◽  
pp. 371-379 ◽  
Author(s):  
L del Campo ◽  
A Sagredo ◽  
R Aras-López ◽  
G Balfagón ◽  
M Ferrer
Keyword(s):  
Electrical Field Stimulation ◽  
Mesenteric Arteries ◽  
Induced Response ◽  
Field Stimulation ◽  
Sprague Dawley ◽  
Synthesis Inhibitor ◽  
Electrical Field ◽  
Rat Mesenteric Artery ◽  
No Release ◽  
Male Sex

The aim of this study was to analyze whether endogenous male sex hormones influence the release of thromboxane A2 (TXA2) and its role in the electrical field stimulation (EFS)-induced response, as well as the mechanism involved. For this purpose, endothelium-denuded mesenteric arteries from control and orchidectomized male Sprague–Dawley rats were used to measure TXA2 release; EFS-induced response, nitric oxide (NO), norepinephrine (NA), and prostaglandin (PG) I2 release were also measured in the presence of the TXA2 synthesis inhibitor furegrelate. Orchidectomy increased basal and EFS-induced TXA2 release. Furegrelate decreased the EFS-induced contraction in arteries from control rats, but did not modify it in arteries from orchidectomized rats. The EFS-induced neuronal NO release and vasodilator response were increased by furegrelate in arteries from control rats, but were not modified in arteries from orchidectomized rats. Furegrelate did not modify the EFS-induced NA release or vasoconstrictor response in arteries from either control or orchidectomized rats. The EFS-induced PGI2 release was not modified by furegrelate in arteries from control rats, but was increased in arteries from orchidectomized rats. The results of the present study show that endogenous male sex hormone deprivation i) increases non-endothelial TXA2 release and ii) regulates the effect of endogenous TXA2 on the EFS-induced response through different mechanisms that, at the least, involve the NO and PGI2 systems. In arteries from control rats, inhibition of TXA2 formation decreases the EFS-induced response by increasing neuronal NO release. In arteries from orchidectomized rats, the EFS-induced response is unaltered after the inhibition of TXA2 formation, by increasing PGI2 release.

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