gms | German Medical Science

102. Jahrestagung der DOG

Deutsche Ophthalmologische Gesellschaft e. V.

23. bis 26.09.2004, Berlin

Effects of NOS inhibitor L-NMMA and ATII receptor antagonist Candesartan on retinal circulation in young hypertensive patients

Meeting Abstract

  • corresponding author S. Wärntges - Augenklinik, Universität Erlangen-Nürnberg, Erlangen
  • J. Harazny - Augenklinik, Universität Erlangen-Nürnberg, Erlangen
  • C. Delles - Medizinische Klinik IV, Universität Erlangen-Nürnberg, Erlangen
  • S. Oehmer - Medizinische Klinik IV, Universität Erlangen-Nürnberg, Erlangen
  • R.E. Schmieder - Medizinische Klinik IV, Universität Erlangen-Nürnberg, Erlangen
  • G. Michelson - Augenklinik, Universität Erlangen-Nürnberg, Erlangen

Evidenzbasierte Medizin - Anspruch und Wirklichkeit. 102. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft. Berlin, 23.-26.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04dogP 168

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

Published: September 22, 2004

© 2004 Wärntges 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.




Changes of retinal vasculature are among the typical consequential damages of arterial hypertension. But in cases of mild hypertension the explanation of a direct influence of an elevated systemic pressure seems to be insufficient. Thus, other factors such as a deteorated release of nitric oxide (NO), a powerful endothelium-derived vasodilator, may be involved. In the present study we examined the effect of NOS inhibition (nitric oxide synthase) by NG-monomethyl-L-arginine acetate (L-NMMA) on ocular and systemic blood circulation of young hypertensive patients and tested for an interference by angiotensin II (ATII) receptor antagonist candesartan.


Thirteeen hypertensive patients (mean age 28.6±3.5 years) and 15 non-hypertensive controls (mean age 27.7±4.1 years) received candesartan or placebo in a randomized double-blind order. Systemic hemodynamic parameters were registered by using beat-to-beat volume-clamp technique (Portapres) whereas blood velocity of central retinal artery (vACR) was measured by pulsed doppler sonography. Following a washout phase in the second part of the study medication was exchanged and measurements were repeated.


L-NMMA increased mean arterial finger pressure and total peripheral resistance and decreased heart rate and cardiac output highly significant independent of hypertension or therapy with candesartan. In untreated controls vACR was elevated by L-NMMA (6.4 ± 1.2cm/s vs. 8.1 ± 1.8cm/s, p = 0.005) but not in hypertension (6.8 ± 0.6cm/s vs. 7.2 ± 0.3cm/s, p = 0.24). Candesartan had no significant effect on vACR in controls and hypertension before L-NMMA application but it tended to normalize the effect of L-NMMA on vACR in hypertensive patients (all data given as mean ± SD).


In ocular circulation of hypertensive subjects the release of NO is impaired and can be improved by candesartan.