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(Hypertension. 2001;37:293.)
© 2001 American Heart Association, Inc.

Scientific Contributions

Exclusion of the ACE D/I Gene Polymorphism as a Determinant of Endothelial Dysfunction

Gian Paolo Rossi; Stefano Taddei; Agostino Virdis; Lorenzo Ghiadoni; Giovanna Albertin; Stefania Favilla; Isabella Sudano; Achille C. Pessina; Antonio Salvetti

From the Departments of Internal Medicine (S.T., A.V., L.G., S.F., I.S., A.S.) and Clinical and Experimental Medicine (G.P.R., A.C.P.), University of Pisa, Pisa, Italy; and Clinica Medica 4 and Human Anatomy and Physiology (Section of Anatomy) (G.A.), University of Padova, Padova, Italy.

Correspondence to Gian Paolo Rossi, MD, FACC, Department of Clinical and Experimental Medicine, Clinica Medica 4, University Hospital, via Giustiniani, 2, 35126 Padova, Italy. E-mail gprossi{at}ux1.unipd.it

A deletion/insertion (D/I) polymorphism within the ACE gene may increase the risk of cardiovascular events through still unknown mechanisms. The latter may involve increased angiotensin II–induced NO breakdown and/or reduced agonist-mediated NO release. We therefore investigated whether the D allele of the ACE gene affects endothelium-dependent vasodilatation in mild-to-moderate primary hypertensive patients and healthy normotensive subjects. We compared in a cross-sectional study the forearm blood flow response of the 3 D/I genotypes with 5 incrementally increasing doses of the endothelium-dependent vasodilator acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 µg · 100 mL^-1 · min^-1) in 142 subjects: 103 mild-to-moderate uncomplicated primary hypertensives (49.3±9.1 years old, 152±11/99±5 mm Hg) and 39 normotensives (44.6±15.3 years old, 122±12/78±6 mm Hg). We also assessed the endothelium-independent vasodilatation in the forearm, as blood flow response to 3 incrementally increasing doses of sodium nitroprusside (1, 2, and 4 µg · 100 mL^-1 · min^-1). The overall genotype distribution was II, n=10; ID, n=70; and DD, n=62. It did not differ significantly between primary hypertensives and normotensives. A significant blunting of endothelium-dependent vasodilatation in primary hypertensive patients compared with normotensive subjects (P<0.001) was found. No effect of the DI genotype on endothelium-dependent and -independent vasodilatation was detected. Thus, these results obtained in a relatively large population do not support the contention that the D allele is associated with a blunting of either stimulated endothelial NO or donated NO responses in both mild-to-moderate primary hypertensive patients and normotensive subjects.

Key Words: hypertension, arterial • gene expression • kininase II • nitric oxide • vasodilatation

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