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Am J Physiol Regul Integr Comp Physiol 281: R878-R886, 2001;
0363-6119/01 $5.00
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Vol. 281, Issue 3, R878-R886, September 2001

Mineralocorticoids upregulate arterial contraction to epidermal growth factor

Jennifer A. Florian1, Anne Dorrance2, R. Clinton Webb2, and Stephanie W. Watts1

1 Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan 48824 - 1317; and 2 Department of Physiology, Medical College of Georgia, Augusta, Georgia 30912

The present studies test the hypothesis that contraction to EGF is dependent on mineralocorticoids and/or an elevation in systolic blood pressure (SBP). Endothelium-denuded thoracic aortas from sham normotensive, Nomega -nitro-L-arginine (L-NNA) hypertensive, Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR) were used in isolated tissue-bath experiments. Maximal contraction to epidermal growth factor [EGF; percentage of phenylephrine (PE; 10 umol/l)-induced contraction] was greater in strips from L-NNA (32 ± 5%) and SHR (53 ± 8%) rats compared with sham and WKY rats (17 ± 1 and 12 ± 4%, respectively). Wistar-Furth rats became only mildly hypertensive when given DOCA salt (134 ± 6 mmHg) compared with Wistar rats (176 ± 9 mmHg), but aortas from both strains had a similarly enhanced contraction to EGF (~9 times the maximal contraction of sham aorta). Furthermore, in vitro incubation of aortas from Wistar and Wistar-Furth rats with aldosterone (10 nmol/l) increased EGF-receptor mRNA expression by >50%. These data indicate that arterial contraction to EGF may occur independent of hypertension and be stimulated by mineralocorticoids.

hypertension; vascular smooth muscle contraction; Wistar/Wistar-Furth rats


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