CHRONIC BLOCKADE OF NITRIC-OXIDE SYNTHESIS ELEVATES PLASMA-LEVELS OF CATECHOLAMINES AND THEIR METABOLITES AT REST AND DURING STRESS IN RATS

Formation of nitric oxide, an endothelium-derived relaxing factor, can be inhibited by administration of N-nitro-L-arginine methylesther (L- NAME). In the present study, the activity of the sympathoadrenal syste m in rats with blood pressure (BP) elevation induced by L-NAME was inv estigated. L-NAME was administered in a dose of 50 mg/kg, i.p. every 1 2 h for 4 days. Blood samples were collected via chronically inserted arterial catheters in conscious, freely moving rats at rest and during immobilization stress. Plasma epinephrine (EPI), norepinephrine (NE), and dopamine (DA), as well as catecholamine metabolites dihydroxyphen ylglycol (DHPG) and dihydroxyphenylacetic acid (DOPAC) were measured b y HPLC method. In L-NAME treated animals, which showed a significant i ncrease in BP, plasma EPI levels were markedly elevated both before an d during stress. Plasma NE levels were not significantly increased, ho wever, DHPG levels, which indicate NE turnover and reuptake, were high ly elevated. Plasma DA levels were not changed after L-NAME administra tion but DA metabolite DOPAC showed a significant elevation both under basal conditions and during stress. Thus, the present results indicat e that the prolonged blockade of nitric oxide synthesis that causes ar terial hypertension is associated with an activation of the sympathoad renal system.