Low levels of lead, but not high levels, produce hypertension. This mystery
has not yet been resolved. In this study we compared the in vitro vasoresp
onsiveness in rat thoracic aorta to low dose (10(-8) mol/L) and high dose (
10(-5) mol/L and 10(-4) mol/L) lead acetate. In addition to the direct resp
onse to lead, we examined reactivity to norepinephrine, acetylcholine, isop
roterenol, phorbol ester, and calcium in the presence and absence of lead.
Neither low-dose nor high-dose lead directly affected aortic contractile or
relaxant responses. However, lead, only at the highest concentration (10-4
mol/L), increased the contractions to calcium at all submaximal calcium co
ncentrations. We conclude that low-dose lead must increase blood pressure i
ndirectly through a humoral effect. The reasons for the failure of high-dos
e lead to influence blood pressure remain to be explored. (C) 2001 American
Journal of Hypertension, Ltd.