Key result
L-arginine treatment partially reduced the marked increase in monocyte adhesion to carotid endothelium and prevented the impaired release of nitric oxide in rats with salt-sensitive hypertension.
Why the study?
Does L-arginine reduce monocyte adhesion to endothelium in Dahl rats with salt-sensitive hypertension?
Does L-arginine reduce monocyte adhesion to endothelium in Dahl rats with salt-sensitive hypertension?
In a rat model of salt-sensitive hypertension, L-arginine supplementation reduces increased monocyte-endothelial adhesion and partially restores nitric oxide production.
Hypothesis-generating for L-arginine in salt-sensitive hypertension models; human trials needed before any clinical consideration.
Although adhesion of monocytes to endothelial cells is considered as one of the initial factors leading in the long term to the development of atherosclerosis, the effects of hypertension on monocyte-endothelial cell interactions are still largely unknown. Thus we evaluated whether hypertension affects adhesion of monocytes on rat carotid endothelium, and whether this adhesion may be modified by long-term treatment with L-arginine, the physiologic precursor of nitric oxide (NO). Hypertension was induced in Dahl rats using a sodium-rich diet (8%), in the absence or the presence of L-arginine (1.25 g/L in drinking water). After 1 month, the carotid arteries were isolated, opened longitudinally, and incubated in the presence of 2 x 10(6) monocytes previously rendered fluorescent by incubation with tetramethyl rhodamine isothiocyanate (TRITC), and adherent cells were counted under fluorescence microscopy. In parallel, the production of NO was evaluated in vitro in isolated aorta and isolated hearts. Hypertension markedly increased adhesion of monocytes on carotid endothelium, and this was reduced by L-arginine. Hypertension also reduced an index of NO release at the level of the aorta and the coronary circulation. This impaired release of NO was partially prevented by L-arginine. Thus hypertension was associated with an increased adhesion of monocytes, which is probably due at least in part to a decreased production of NO. The increased adhesion was partly reduced by L-arginine, possibly secondary to an increased production of NO. Such an increased adhesion of monocytes may contribute the increased cardiovascular risk in hypertension.
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Artigues et al. (2000) studied Salt-Sensitive Hypertension. L-arginine vs. Absence of L-arginine was evaluated on Adhesion of monocytes on rat carotid endothelium and NO production. L-arginine treatment partially reduced the marked increase in monocyte adhesion to carotid endothelium and prevented the impaired release of nitric oxide in rats with salt-sensitive hypertension.