Renal effects of an acute NaCl load in chronic nitric oxide blockade-induced hypertensive rats

Nitric oxide (NO) controls blood pressure and plays a role in the water and sodium handling by the kidneys. Inhibition of NO synthesis with competitive L-arginine analogues leads to increased renal vascular resistance and raised systemic and glomerular blood pressure. The effects of chronic NO-synthesis inhibition by N(G)-nitro L-arginine methyl-esther (L-NAME) in the disposal of an acute NaCl load are studied on fourteen male Munich-Wistar rats. Eight of which were given L-NAME (100 mg/L) in the drinking water for 21 days. Six control rats differed only in not receiving L-NAME. As expected, significant hypertension and a marked renal vasoconstriction were accompanied by a decline in renal plasma flow, without changes in glomerular filtration rate, with filtration fraction thus being increased in the NO-blocked rats. In the basal state there was no significant reduction of sodium urinary excretion in the L-NAME treated rats. Both groups of rats elicited an increase in urinary sodium excretion after the NaCl load which was initially more evident and longer in the L-NAME treated group. The ratio of Na+ excreted to Na+ infused was similar between the groups. This observation suggests that in this model of chronic inhibited NO rats, the disposal of an acute sodium load is reached. The existence of a delayed mechanism in renal excretion of Na+ by the chronic NO-blocked rats could be suggested.