In vivo and in vitro effects of lead on vascular reactivity in rats.

R. C. Webb, R. J. Winquist, W. Victery, A. J. Vander

Research output: Contribution to journalArticle

67 Citations (Scopus)

Abstract

The effects of lead on vascular responsiveness were examined in rats. Adult rats, which had received levels of lead acetate in their drinking water to produce blood levels similar to those seen in some urban human populations, consistently had higher systolic blood pressures compared to age-matched controls. Helical strips of tail arteries from the lead-treated rats displayed a greater force-generating ability in response to the cumulative addition of methoxamine to the muscle bath. There were no differences in ED50 between the two groups. Similar results were obtained when norepinephrine was used. The calcium-entry blocker, D 600, was less effective in reducing in reducing contractions induced by methoxamine in lead-treated rats than in controls. There were no differences between the two groups in responses to KCl or electrical stimulation of nerve endings. Contractile responses to norepinephrine, methoxamine, KCl, and nerve stimulation in arteries from untreated rats were unaltered by addition of lead acetate to the muscle bath. These results demonstrate that hypertension induced by moderate levels of lead intake is associated with an increased vascular responsiveness to alpha-adrenergic agonists.

Original languageEnglish (US)
Pages (from-to)H211-6
Number of pages6
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume241
Issue number2
StatePublished - Aug 1 1981

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Blood Vessels
Methoxamine
Baths
Norepinephrine
Arteries
Adrenergic alpha-Agonists
Gallopamil
Hypertension
Muscles
Urban Population
Nerve Endings
Drinking Water
Electric Stimulation
Tail
Lead
In Vitro Techniques
Blood Pressure
Calcium
lead acetate

ASJC Scopus subject areas

  • Physiology

Cite this

In vivo and in vitro effects of lead on vascular reactivity in rats. / Webb, R. C.; Winquist, R. J.; Victery, W.; Vander, A. J.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 241, No. 2, 01.08.1981, p. H211-6.

Research output: Contribution to journalArticle

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