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

AX5-69
Reference
Carmignani
et al. (1999)
Sharifi et al.
(2004)
Gonick at al.
(1998)
Dorman and
Freeman
(2002)
Giridhar and
Isom (1990)
Table AX5-5.4. Studies of the Effects of Lead Exposure on Renin-angiotensin System, Kallikrein-Kinin System,
Prostaglandins, Endothelin, and Atrial Natriuretic Peptide (ANP)
Species/
Tissue
Pb Exposure Measured Parameters
Age/
Weight n Dosage Duration Pb Level CVS Other Interventions Results
Male SD rats Weaning 16 Pb acetate
60 ppm
drinking water
Male SD rats 200 g 32 Pb acetate
100 ppm
drinking water
Male SD rats 2 mo 21 Pb acetate
100 ppm
drinking water
VSMC
(rat aorta)
— — 0.0, 0.02, 0.2,
2.0 mg/dL
Male SD rats 150–175 g 20 Pb acetate 0.01,
0.01, 0.5, 1.0
mg/Kg, BiW, IP
10 mo Blood 24.2 ±
1.8 µg/dL
BP, HR, carotid
blood flow
Plasma ACE,
Kininase Kallikrein
activities dp/dt
2–8 wks — BP ACE activity in
plasma, aorta, heart,
kidney
12 wks — BP Urinary Tx B2, 6keto
PGF1
up to 48 hrs 0.0 to 2
mg/dL
— Arachidonic acid
(AA), DNA
synthesis, cell
proliferation + cell
viability
— Pb exposure raised BP
and dp/dt, lowered carotid
blood flow without
changing HR. This was
associated with marked
increase in plasma ACE,
Kininase II and Kininase I
activities.
— Pb exposure raised BP,
ACE activity in plasma
and tested tissues
markedly increased
peaking within 2–4 wks
followed by a decline to
subnormal values.
— Pb exposure raised BP but
did not affect urinary PG
metabolite excretion
rates.
Ang II, FCS Pb augmented Ang II
stimulated AA release in
a concentrationdependent
fashion. At
low concentrations, Pb
augmented Ang IIstimulated
DNA synthesis
and lowered cell count in
unstimulated cells.
30 days — — ANF — Pb exposure resulted in
fluid retention (↓urine
flow + unchanged fluid
intake + weight gain).
This was associated with
decreased plasma and
hypothalamic ANF levels
.