gms | German Medical Science

29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Hochdruckliga e. V. DHL ® - Deutsche Hypertonie Gesellschaft Deutsches Kompetenzzentrum Bluthochdruck

23. bis 25.11.2005, Berlin

Increased neuronal nitric oxide synthase expression in the hypothalamus of spontaneously hypertensive rats: a counter-regulatory mechanism to hypertension?

Erhöhte Expression der neuronalen NO Synthase im Hypothalamus spontan hypertensiver Ratten: ein Gegenregulationsmechanismus bei der Hypertonie?

Meeting Abstract

  • A. Mischnik - Universitätsklinikum Schleswig-Holstein, Campus Lübeck (Lübeck, D)
  • W. Häuser - Universitätsklinikum Schleswig-Holstein, Campus Lübeck (Lübeck, D)
  • F. Qadri - Universitätsklinikum Schleswig-Holstein, Campus Lübeck (Lübeck, D)
  • N. Wasilewski - Universitätsklinikum Schleswig-Holstein, Campus Lübeck (Lübeck, D)
  • P. Dominiak - Universitätsklinikum Schleswig-Holstein, Campus Lübeck (Lübeck, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP80

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

Published: August 8, 2006

© 2006 Mischnik 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.



Blockade of central nitric oxide synthase, specifically neuronal (nNOS), further increased mean arterial blood pressure of spontaneously hypertensive rats (SHR). We hypothesize that increased nitric oxide (NO) synthesis in the brain may be compensatory to hypertension.

The hypothalamus is the important neuroendocrine regulatory region with respect to blood pressure control, and a large number of neurons possess nNOS. Therefore, nNOS gene expression was measured in adult SHR hypothalamus and compared with age-matched Wistar-Kyoto (WKY) rats. In addition, nNOS expression was analyzed in SHR treated with different antihypertensive drugs. Furthermore, the expression was also studied in 2-kidney-1-clip renal hypertensive rats (2K1C) to investigate whether changes in nNOS expression are characteristic of genetic hypertension or are secondary to blood pressure elevation.

The nNOS mRNA and protein levels were significantly higher in SHR when compared to age-matched WKY rats. Four weeks treatment of SHR with enalapril (an ACE inhibitor) did not change nNOS mRNA but decreased protein levels. Candesartan (an AT1-receptor antagonist) and hydralyzin (a peripheral vasodilator) also had also no effect on mRNA expression but elevated nNOS protein levels. The nNOS mRNA levels were not different in 2K1C rats at three time points, i.e. 48 h, 3 and 6 weeks following clipping the renal artery when compared to sham operated rats.

Upregulation of nNOS gene expression in the hypothalamus of SHR may be involved in the pathogenesis of hypertension and is characteristic of genetic hypertension. The differential nNOS protein expression following treatment with different antihypertensive drugs contribut in lowering blood presure through different compensatory mechanisms.