Nitric oxide produced both by platelet and endothelium increases cGMP leading to vasodilatation and inhibition of platelet aggregation1,2. A reduction of nitric oxide (NO) synthesis may contribute to the impaired endothelium-dependent vasodilatation and platelet activation observed in essential hypertension1,2. Both pathological alterations are associated with increased atherothrombotic events. In the present study, we investigated the effects of hypertension on the L-arginine-NO pathway in human platelets. A total of 8 patients with essential hypertension and 9 healthy subjects participate in the study. The measurement of platelet NOS activity, was determined by the conversion of L-[³H] arginine to L-[³H] citrulline. The levels of intracellular platelet cGMP content was determined in washed platelets by a EIA kit (Cayman). Aggregation was induced by collagen (4mg/ml) and was monitored for 5 min. in a dual channel aggregometer. The platelet aggregation in response to collagen were increased in hypertensive patients (92 ± 3 %) compared to control (81 ± 0.5 %). The L-arginine transport via system y⁺L (pmol/10⁹cells/min) and basal L-citrulline production (pmol/10⁸cells) were reduced in hypertensive patients (34 ± 14 and 0.1 ± 0.01) compared with control (86 ± 17 and 0.21 ± 0.01). Basal platelet cGMP (pmol/10⁸cells) was also impaired in hypertension (0.1 ± 0.03 vs 0.21. ± 0.09, p<0.05). Our findings provide evidence that platelet aggregation is activated in hypertensive patients. It is possible that a reduction in L-arginine transport leading to an impaired NO production is behind the increased platelet aggregation present in hypertension. These data confirm the link between hypertension and altered platelet function and suggest a role for NO in hypertensive cardiovascular thrombotic events.