Air Quality Criteria for Lead Volume II of II - (NEPIS)(EPA) - US ...

AX5-70
Reference
Shelkovnikov
and Gonick
(2001)
Purdy et al.
(1997)
Oishi et al.
(1996)
Valencia et al.
(2001)
Species/
Tissue
Table AX5-5.5. Studies of Effect of Lead on Vascular Contractility
Pb Exposure Measured Parameters
Age/
Weight n Dosage Duration Pb Level CVS Other Interventions Results
Rat aorta rings Pb acetate
10 −8 to 10 −4
Male SD rats 8 wks Pb acetate 100
ppm in water
Male Wistar
rats
Wistar rat
thoracic aorta
rings
7 wks 6 sets/
experiment
Short
incubations
— Vasoconstriction/
vasodilation
3 mo — BP Aorta ring
response to NE,
phenylephrine,
acetylcholine, and
nitroprusside
Pb acetate 1–3 mo Mesenteric art
and aorta
response to
acetylcholine in
presence or
absence of NOS
inhibitor (L-
NAME)
Pb acetate
0.1–3.1 mM
Rapid
response
in vitro
— In vitro
contractile
response
Pb acetated did not cause
vasoconstriction and did
not modify the response
to NE, isoproterenol,
phorbol ester or
acetylcholine but raised
contractile response to
submaximal Ca 2+
concentration
Pb exposure raised BP.
Aorta ring
vasoconstrictive response
to NE and phenylephrine
and vasodilatory
response to acetylcholine
and nitroprusside were
unchanged.
Vasorelaxation response
to acetylcholine in
presence of L-NAME
was significantly reduced
in mesenteric art, but not
aorta of Pb-exposed
animals (Inhibition of
hyperpolarizing factor)
Pb induced a
concentration-dependent
vasoconstriction in intact
and endothelial-denuded
rings in presence or
absence of α-1 blocker,
PKC inhibitor, L. type
Ca 2+ channel blocker or
intra- and extracellular
Ca 2+ depletion.
However, the response
was abrogated by
lanthanum (a general Ca
channel blocker)