Adhesion of monocytes to endothelial cells is considered as one of the initial factors leading on the long term to the development of atherosclerosis. We evaluated whether hypertension affects adhesion of monocytes on rat carotid endothelium, and whether this adhesion may be modified by a chronic treatment with L-arginine, the physiological 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 mg/kg/day). After 1 month, the carotid arteries were isolated, opened longitudinally, and incubated in the presence of monocytes previously rendered fluorescent by incubation with tetramethyl rhodamine isothiocyanate (TRITC), and adherent cells were counted under fluorescence microscopy. Monocyte adhesion was minimal in carotid arteries isolated from normotensive rats (13 +/- 5, n = 8). Hypertension induced a marked, significant increase in monocyte adhesion (97 +/- 17; n = 10; p < 0.01 vs normotensive). This increased adhesion was significantly reduced by chronic treatment with L-arginine (37 +/- 13; n = 12, p < 0.05 vs untreated hypertensive). Thus, hypertension was associated with an increased adhesion of monocytes, which is probably due to a decrease production of NO. The increased adhesion was partly prevented by L-arginine, possibly secondary to an increased production of NO. Such an increased adhesion of monocytes may contribute to the increased cardiovascular risk in hypertension.