Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2004 Mar 19;488(1-3):147-55.
doi: 10.1016/j.ejphar.2004.02.014.

Prenatal stress changes rat arterial adrenergic reactivity in a regionally selective manner

Affiliations

Prenatal stress changes rat arterial adrenergic reactivity in a regionally selective manner

Marijke Sanders et al. Eur J Pharmacol. .

Abstract

A suboptimal fetal environment has been linked to increased risk of cardiovascular disease in adulthood. We investigated whether intrauterine stress (IUS) alters the development of adrenergic reactivity in different types of rat arteries. Intrauterine stress was induced by ligation of the uterine arteries at day 13 of pregnancy in Wistar rats. First-order mesenteric, renal, femoral and saphenous arteries of the 21-day-old male offspring were studied in a myograph. IUS in the rat changes arterial adrenergic reactivity in a regionally selective manner. Adrenoceptor-mediated responses are altered in the renal artery. Maximal contractile responses to phenylephrine were increased, while sensitivity to the alpha(1)-adrenoceptor agonist was decreased. Intrauterine stress significantly reduced contractile responses to norepinephrine and enhanced relaxing responses to isoproterenol in the renal artery. Adrenergic responses were not modified in mesenteric, femoral and saphenous arteries. In the kidneys the densities of [(3)H]prazosin binding sites, periarterial adrenergic nerves and of the glomeruli were not altered after intrauterine stress at day 13 of gestation. The observed regionally selective alterations in arterial reactivity might link a suboptimal fetal environment to the development of cardiovascular disease in the adult.

PubMed Disclaimer

MeSH terms

LinkOut - more resources