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(Hypertension. 2001;38:1337.)
© 2001 American Heart Association, Inc.

Scientific Contributions

Arterial Epidermal Growth Factor Receptor Expression in Deoxycorticosterone Acetate–Salt Hypertension

Carrie Northcott; Jennifer A. Florian; Anne Dorrance; Stephanie W. Watts

From the Department of Pharmacology and Toxicology, Michigan State University (C.N., J.F., S.W.), East Lansing; and Department of Physiology, Medical College of Georgia (A.D.), Augusta.

Correspondence to Stephanie W. Watts, B445 Life Sciences Bldg, Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824-1317. E-mail wattss{at}msu.edu

Epidermal growth factor (EGF) causes contraction in arteries from deoxycorticosterone acetate (DOCA)–salt hypertensive rats but not in normotensive sham rats. We hypothesized that an increase in the number of EGF receptors (EGFRs) in arteries from DOCA-salt rats enables the observed contraction to EGF to occur. DOCA-salt rats had a systolic blood pressure >170 mm Hg, whereas all sham rats had a systolic blood pressure <125 mm Hg. Thoracic aorta were removed for measurement of isometric force, EGFR mRNA levels, and EGFR protein levels. EGF caused a significant contraction in endothelium-denuded aorta from DOCA-salt rats (38±7% of maximal phenylephrine-induced [10 µmol/L] contraction) compared with aorta from sham rats (4±2%). The EGFR tyrosine kinase–specific inhibitors 4,5-dianilinophthalimide (10 µmol/L) and AG1478 (250 nmol/L) reduced contraction in aorta from DOCA-salt by 85±14% and 65±10%, respectively. EGFR mRNA in DOCA-salt aorta was increased 4.2-fold compared with that in sham aorta. However, Western analyses of membrane-enriched and whole-tissue lysate of aorta from sham and DOCA-salt revealed no statistical difference in the density of EGFR protein between sham and DOCA-salt aorta. These data refute our hypothesis and suggest that a change downstream of EGFR is responsible for enabling EGF-induced contraction in hypertension.

Key Words: EGF • mineralocorticoid • artery • tyrosine kinase

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