Mineralocorticoids upregulate arterial contraction to epidermal growth factor

The present studies test the hypothesis that contraction to EGF is dependen t on mineralocorticoids and/or an elevation in systolic blood pressure (SBP ). Endothelium-denuded thoracic aortas from sham normotensive, N-omega-nitr o-L-arginine (L-NNA) hypertensive, Wistar-Kyoto (WKY), and spontaneously hy pertensive rats (SHR) were used in isolated tissue-bath experiments. Maxima l 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 mm Hg), but aortas from both strains had a similarly enhanced contraction to E GF (similar to9 times the maximal contraction of sham aorta). Furthermore, in vitro incubation of aortas from Wistar and Wistar-Furth rats with aldost erone (10 nmol/l) increased EGF-receptor mRNA expression by >50%. These dat a indicate that arterial contraction to EGF may occur independent of hypert ension and be stimulated by mineralocorticoids.