Mineralocorticoids upregulate arterial contraction to epidermal growth factor

Abstract

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, N ω-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.