Haloperidol-sensitive relaxation of the rat mesenteric artery to electrical field stimulation

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

Clinical Science ◽

10.1042/cs20110072 ◽

2011 ◽

Vol 121 (8) ◽

pp. 331-341 ◽

Cited By ~ 18

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.

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