Small doses of mercury increase arterial pressure
reactivity to phenylephrine in rats
Adriana Caiado Machado a , Alessandra Sim˜ o Padilha a , Giulia Alessandra Wiggers a ,
a , Ivanita Stefanon a,b , Dalton Valentim Vassallo a,b,∗
Fabiana Dayse Magalh˜ es Siman
Department of Physiological Sciences, Federal University ofEspirito Santo, Vitoria, ES, Brazil
b Health Science Center of Vit´ ria-EMESCAM, Vitoria, ES, Brazil
Received 7 November 2005; accepted 12 February 2007
Available online 21 April 2007
Mercury reduces cardiac contractility and arterial pressure at micromolar concentrations. We investigated the actions of 680 ng/kg HgCl2 on
arterial pressure, heart rate (HR) and on the pressorreactivity to phenylephrine (PHE) in rats before and 1 h after HgCl2 administration and after
hexametonium, verapamil and tempol treatments. HgCl2 increased baseline systolic (SAP) and diastolic pressure (DAP) and HR, sensitivity (pD2 )
and maximal response (Emax ) to PHE pressor reactivity. Hexametonium and verapamil reduced baseline pressures and HR that increased after HgCl2
treatment.Hexametonium did not change pD2 or Emax to PHE but verapamil reduced them. These parameters increased after HgCl2 administration.
Tempol did not alter baseline pressures, HR or PHE reactivity before and after HgCl2 . Results suggest that HgCl2 increases SAP, DAP, HR and
PHE reactivity; autonomic reﬂexes reduces HgCl2 action; baseline pressure level do not interfere on HgCl2 pressor effects but freeradicals seems
to be involved.
© 2007 Elsevier B.V. All rights reserved.
Keywords: Mercury; Pressure reactivity; Arterial pressure; Phenylephrine
Acute intravenous administration of Hg2+ produces important hemodynamic changes. The main effect is a progressive
decrease of arterial blood pressure (ABP) associated with the
reduction of heart rate (HR) (Rhee and Choi, 1989;Massaroni et
al., 1995). The cardio toxicity and a decreased cardiac mechanical activity induced by inorganic mercury could explain this
ABP reduction (Rhee and Choi, 1989; Halbach, 1990; Oliveira
et al., 1994; Massaroni et al., 1995). Regarding its vascular
effects, previous reports showed that HgCl2 concentrations from
0.5 to 10 M induced vasoconstriction, reduced the endothelial vasodilatoractivity decreasing the bioavailability of nitric
oxide and stimulating a COX-derived vasoconstrictor pathway
(Da Cunha et al., 2000).
∗ Corresponding author at: Departamento de Ciˆ ncias Fisiol´ gicas,
CBM/UFES, Av. Marechal Campos, 1468, Maru´pe, 29040-095 Vit´ ria, ES,
Brazil. Tel.: +55 27 33357350; fax: +55 27 33357330.
E-mail address: email@example.com (D.V. Vassallo).1382-6689/$ – see front matter © 2007 Elsevier B.V. All rights reserved.
Previous reports suggested that cardiac and vascular effects
might be observed after continuous exposure to very small concentrations of mercury (Assis et al., 2003). It was also reported
that professional exposure to mercury vapor and the release
of mercury from or during removal ofamalgam dental ﬁllings increases its blood and plasma concentration (Halbach,
1995; Bj¨ rkman et al., 1997; Langworth et al., 1997; Sandborgho
Englund et al., 1998). After exposure to mercury vapor, blood
concentration attains 18 nmol/l (Langworth et al., 1997) and
after exposure to dental and removal of amalgam ﬁllings, plasma
concentration attains 5 nmol/l (Bj¨ rkman et al., 1997). Profesosional exposure also produces central nervous system alteration
(Langworth et al., 1997; Oliveira et al., 1994; Aschner and
Aschner, 1990) and amalgam tooth ﬁllings impair sheep kidney
function (Carmignani et al., 1989).
However, there are no reports showing that the administration of small doses of mercury, which produces concentrations
similar to those, found in the blood or plasma after...