gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

Hydrochlorothiazide attenuates agonist-induced vasoconstriction by affecting Rho kinase

Hydrochlorothiazid schwächt die durch Agonisten induzierte Vasoconstriction durch Einfluss auf die Rho kinase

Meeting Abstract (Hypertonie 2004)

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  • Z. Zhu - Chongqing, VCR
  • S. Zhu - Chongqing, VCR
  • T. Cao - Chongqing, VCR
  • D. Liu - Chongqing, VCR
  • L. Wang - Chongqing, VCR
  • M. Tepel - Charité Camput Benjamin Franklin, Department of Hypertension and Endocrinology Berlin

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP10

The electronic version of this article is the complete one and can be found online at:

Published: August 10, 2005

© 2005 Zhu et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Objective: Lowering blood pressure using hydrochlorothiazide has been proven to be effective in clinical studies. The mechanisms by which hydrochlorothiazide lowers blood pressure is still poorly understood

Methods: To evaluate whether hydrochlorothiazide causes calcium desensitization in smooth muscle cells we measured its effects on agonist-induced increase of blood pressure in Wistar rats in vivo, and on agonist-induced vasoconstriction of aortic rings, RhoA, Rho kinase, and intracellular calcium in vascular smooth muscle cells in vitro.

Results: Hydrochlorothiazide significantly attenuated angiotensin II-induced increase of systolic blood pressure in rats from 26±17 mmHg to 2±1 mmHg (mean±SD, n=5, p<0.05). Hydrochlorothiazide inhibited agonist-induced vasoconstriction of aortic rings in a concentration-dependent manner. The incubation of segments from rat aorta with 1 µmol/L hydrochlorothiazide significantly reduced the angiotensin II-induced vasoconstriction to 22±18% (n=6; p<0.01). The inhibitory effect of hydrochlorothiazide was observed both in the presence and absence of endothelium. RT-PCR and immunoblotting showed that RhoA and Rho kinase were significantly reduced in vascular smooth muscle cells after administration of hydrochlorothiazide to 38±17% and to 36±3%, respectively (p<0.05). Agonist-induced changes of intracellular calcium were not affected by hydrochlorothiazide.

Conclusion: The study indicates that hydrochlorothiazide inhibits agonist-induced vasoconstriction by calcium desensitization in smooth muscle cells linked to the Rho kinase pathway