Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 2004;43:36-40
Published online before print December 1, 2003, doi: 10.1161/01.HYP.0000103868.45064.81
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
43/1/36    most recent
01.HYP.0000103868.45064.81v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cardillo, C.
Right arrow Articles by Panza, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cardillo, C.
Right arrow Articles by Panza, J. A.

(Hypertension. 2004;43:36.)
© 2004 American Heart Association, Inc.


Scientific Contributions

Enhanced Vascular Activity of Endogenous Endothelin-1 in Obese Hypertensive Patients

Carmine Cardillo; Umberto Campia; Micaela Iantorno; Julio A. Panza

From the National Heart, Lung, and Blood Institute (C.C., U.C., J.A.P.), Bethesda, Md; Università Cattolica del Sacro Cuore (C.C., M.I.), Rome, Italy; and Washington Hospital Center (U.C., J.A.P.), Washington, DC.

Correspondence to Dr Julio A. Panza, Washington Hospital Center, 110 Irving St NW, Suite 2A 74, Washington, DC 20010. E-mail julio.a.panza{at}medstar.net

Hypertensive patients have increased endothelin-1–dependent vasoconstrictor tone. This abnormality, however, might not be uniformly present in all forms of hypertension, as suggested by experimental studies showing that endothelin-1 activity is enhanced predominantly in low-renin, high-volume models and in insulin-resistant states. Because hypertension in obesity is commonly associated with both expanded plasma volume and insulin resistance, this study sought to determine whether increased body mass index (BMI) in hypertensive patients relates to activation of the endothelin-1 system. Forearm blood flow (FBF) responses (plethysmography) to intra-arterial infusion of an ETA receptor blocker (BQ-123) were analyzed in hypertensive patients and normotensive control subjects according to BMI. The vasodilator response to BQ-123 was significantly higher in hypertensive patients than in control subjects (P<0.001). During BQ-123, a significant increase in FBF from baseline was observed in obese (BMI >=30 kg/m2; P<0.001) and overweight (BMI, 27 to 29.9 kg/m2; P=0.04) but not in lean (BMI <27 kg/m2; P=0.83) hypertensive patients. In contrast, no significant change in FBF was observed during BQ-123 either in obese (P=0.53), overweight (P=0.76), or lean (P=0.93) normotensive subjects. Moreover, a significant correlation between BMI and the vasodilator response to ETA blockade was observed in hypertensive subjects (R=0.53; P=0.005) but not in control subjects (R=0.11; P=0.58). In human hypertension, increased BMI is associated with enhanced ETA-dependent vasoconstrictor activity, suggesting that this abnormality may play a role in the pathophysiology of obesity-related hypertension and that targeting the endothelin-1 system may be useful in the treatment of these patients.


Key Words: endothelin • hypertension, obesity • vasculature • atherosclerosis