Aims: 

The question whether endothelial dysfunction is a consequence or a cause of hypertension remains still opened. The aim of this study was to investigate nitric oxide (NO) production and L-NAME-sensitive component of endothelium-dependent vasorelaxation in adult normotensive Wistar-Kyoto (WKY), borderline hypertensive (BHR) and spontaneously hypertensive rats (SHR).

Methods: 

Blood pressure (BP) was determined using tail-cuff plethysmography. Nitric oxide synthase (NOS) activity was determined by conversion of [³H]-L-arginine in the aorta. L-NAME-sensitive component of vasorelaxation was investigated in the preconstricted femoral arteries using the wire myograph during isometric conditions as a difference between acetylcholine (ACh)-induced vasorelaxation before and after acute NOS inhibitor N^G-nitro-L-arginine methyl ester pre-treatment (L-NAME, 10^-5 mol/l).

Results: 

BP of WKY, BHR and SHR was 111 ± 3, 140 ± 4 and 184 ± 6 mmHg, respectively. NOS activity was significantly higher in the aorta of BHR and SHR vs. WKY. ACh-induced vasorelaxation of SHR was significantly greater than that in WKY. There was a significant positive correlation between BP and L-NAME-sensitive component of vasorelaxation of the femoral artery (r = 0.614, p < 0.007).

Conclusion: 

Results suggest the absence of endothelial dysfunction in the femoral artery of adult borderline and spontaneously hypertensive rats and gradual elevation of L-NAME-sensitive component of vasorelaxation with increasing BP. This suggests that reduction of cardiovascular NO production and endothelial dysfunction do not participate in the initiation of hypertension in these experimental models.

Supported by the grants APVT-51-018004 and VEGA 2/7064/27.