Objective: The acute and chronic blockade of Nitric oxide synthase (NOS) enzyme by N^ω-nitro-L-arginine (L-NNA) leads to hypertension. In this model, the co-administration of a high salt diet (1%) increases the intensity of hypertension. The aim of this study is to determine whether salt dependence in this model is related to the extent of nitric oxide inhibition and/or vascular adrenoceptor responsiveness.

Materials and Methods: To determine whether salt dependence in this model is related to the extent of nitric oxide inhibition and/or vascular adrenoceptor responsiveness, we administrated a standard salt, or high salt diet and oral L-NNA treatment to adult male Sprague-Dawley rats at either 5 or 25 mg/kg per day. Blood pressure was measured by using tail-cuff method and urine vanillylmandelic acid (VMA) by High Performance Liquid Chromatography (HPLC) method. Alpha-adrenergic receptor responses in isolated thoracic aorta rings were evaluated in “in vitro” conditions.

Results: Low-dose L-NNA treatment induced a blood pressure augmentation only when associated with sodium overload. In rats receiving high-dose L-NNA, hypertension was aggravated by sodium excess. At the 14^th day of treatment, the urine VMA levels was significantly increased in rats receiving low-dose L-NNA with high salt diet compared with others. Also, vascular alpha-1 adrenergic receptor sensitivity in this group was significantly decreased.

Conclusion: Present findings indicate that the activation of sympathetic may be a main contributor factor to development of hypertension induced by co-administration of a high salt diet with subpressor dose of L-NNA in rats.