This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rizzoni, D. Articles by Agabiti-Rosei, E. Search for Related Content PubMed PubMed Citation Articles by Rizzoni, D. Articles by Agabiti-Rosei, E.

(Hypertension. 1998;31:335.)
© 1998 American Heart Association, Inc.

Scientific Contributions

Endothelial Dysfunction in Hypertension Is Independent From the Etiology and From Vascular Structure

Damiano Rizzoni; Enzo Porteri; Maurizio Castellano; Giorgio Bettoni; Maria Lorenza Muiesan; Guido Tiberio; Stefano M. Giulini; Gianpaolo Rossi; Gianpaolo Bernini; Enrico Agabiti-Rosei

From the Semeiotica and Metodologia Medica (D.R., E.P., M.C., G.B., M.L.M.) and the Chirurgia Generale (G.T., S.M.G.), University of Brescia, the Clinica Medica 1^a (G.R.), Dept. of Clinical and Experimental Medicine, Institute of Clinical Medicine, University of Padua, and the Clinica Medica 1^a (G.B.), University of Pisa, Italy

Correspondence and reprint requests to Damiano Rizzoni, MD, U.O.P. Scienze Mediche, University of Brescia, c/o 1^a Medicina, Spedali Civili, 25100 Brescia, ITALY. E-mail damiano.rizzoni{at}schering-pl.it

The aim of our study was to evaluate the relationships between endothelial function, small resistance artery structure, and blood pressure in patients with primary or secondary hypertension. Sixty subjects were included in the study: 9 patients with pheochromocytoma, 10 with primary aldosteronism, 17 with renovascular hypertension, and 13 with essential hypertension with 11 normotensive subjects who served as controls. Clinic and 24-hour ambulatory blood pressure (ABPM) were evaluated. All subjects were submitted to a biopsy of subcutaneous fat. Small resistance arteries were dissected and mounted on a micromyograph and the media/lumen ratio was calculated. A dose-response curve to acetylcholine was performed at cumulative concentrations from 10^-9 to 10^-5 mol/L. The vasodilator response to acetylcholine was similarly impaired in the four groups of hypertensive patients (ANOVA P<.05 versus normotensive controls), without any significant difference among them. In subcutaneous small arteries of patients with either primary aldosteronism or renovascular hypertension, a marked increase in media:lumen ratio was observed, while in patients with pheochromocytoma, the extent of vascular structural alterations was similar to that observed in essential hypertension. No significant correlation between media-lumen ratio or clinic blood pressure and maximum acetylcholine-induced vasodilatation was observed. On the contrary, a significant, albeit not very close, correlation between ABPM values and maximum acetylcholine-induced vasodilatation was observed (r=34, P<.05 with 24-hour systolic blood pressure, r=0.36, P<.05 with 24-hour diastolic blood pressure). In conclusion, endothelial dysfunction seems to be independent from the degree of vascular structural alterations and from the etiology of hypertension, and it is probably more linked to the hemodynamic load.

Key Words: acetylcholine • endothelium • EDRF • nitric oxide • vascular resistance • hypertrophy • secondary hypertension

Abbreviations: ABPM = ambulatory blood pressure monitoring • ANOVA = analysis of variance • EH = essential hypertensive patients • NT = normotensive subjects • DBP = diastolic blood pressure • ID = normalized internal diameter • MCSA = media cross-sectional area • M/L = media/lumen ratio • MT = media thickness • PA = patients with primary aldosteronism • Phaeo = patients with pheochromocytoma • RVH = patients with renovascular hypertension • SBP = indicates systolic blood pressure • SHR = spontaneously hypertensive rats. • WT = wall thickness

This article has been cited by other articles:

				E. Metaxa, H. Meng, S. R. Kaluvala, M. P. Szymanski, R. A. Paluch, and J. Kolega Nitric oxide-dependent stimulation of endothelial cell proliferation by sustained high flow Am J Physiol Heart Circ Physiol, August 1, 2008; 295(2): H736 - H742. [Abstract] [Full Text] [PDF]

				G. P. Rossi, M. Bolognesi, D. Rizzoni, T. M. Seccia, A. Piva, E. Porteri, G. A.M. Tiberio, S. M. Giulini, E. Agabiti-Rosei, and A. C. Pessina Vascular Remodeling and Duration of Hypertension Predict Outcome of Adrenalectomy in Primary Aldosteronism Patients Hypertension, May 1, 2008; 51(5): 1366 - 1371. [Abstract] [Full Text] [PDF]

				G. P. Rossi, G. Bernini, G. Desideri, B. Fabris, C. Ferri, G. Giacchetti, C. Letizia, M. Maccario, M. Mannelli, M.-J. Matterello, et al. Renal Damage in Primary Aldosteronism: Results of the PAPY Study Hypertension, August 1, 2006; 48(2): 232 - 238. [Abstract] [Full Text] [PDF]

				Y. Higashi, S. Sasaki, K. Nakagawa, H. Matsuura, T. Oshima, and K. Chayama Endothelial Function and Oxidative Stress in Renovascular Hypertension N. Engl. J. Med., June 20, 2002; 346(25): 1954 - 1962. [Abstract] [Full Text] [PDF]

				R. Yang, A. K. Ogasawara, T. F. Zioncheck, Z. Ren, G.-W. He, G. G. DeGuzman, N. Pelletier, B.-Q. Shen, S. Bunting, and H. Jin Exaggerated Hypotensive Effect of Vascular Endothelial Growth Factor in Spontaneously Hypertensive Rats Hypertension, March 1, 2002; 39(3): 815 - 820. [Abstract] [Full Text] [PDF]

				M.-H. Liu, H.-K. Jin, H. S. Floten, Q. Yang, A. P. C. Yim, A. Furnary, T. F. Zioncheck, S. Bunting, and G.-W. He Vascular Endothelial Growth Factor-Mediated Endothelium-Dependent Relaxation Is Blunted in Spontaneously Hypertensive Rats J. Pharmacol. Exp. Ther., April 13, 2001; 296(2): 473 - 477. [Abstract] [Full Text]

				M. Sander, B. Chavoshan, and R. G. Victor A Large Blood Pressure–Raising Effect of Nitric Oxide Synthase Inhibition in Humans Hypertension, April 1, 1999; 33(4): 937 - 942. [Abstract] [Full Text] [PDF]