EFFECTS OF L-NAME ON CEREBRAL METABOLIC, VASOPRESSIN, OXYTOCIN, AND BLOOD-PRESSURE RESPONSES IN HEMORRHAGED RATS

N-G-nitro-L-arginine methyl ester (L-NAME; 250 mu g/5 mu l), an inhibi tor of NO synthase, or the vehicle artificial cerebrospinal fluid (aCS F; 5 mu l) was administered intracerebroventricularly to conscious rat s hemorrhaged (0.7 ml/min) to a 20% volume depletion. Hypotension was maximal 5 min after hemorrhage ended, with compensatory recovery to ba sal levels 20 min later, regardless of drug treatment. L-NAME, however , elevated (P < 0.05) blood pressure (vs. aCSF controls) 40-45 min aft er intracerebroventricular administration. In normovolemic rats, L-NAM E produced a significant presser response and increased plasma levels of vasopressin (VP) and oxytocin (OT). After hemorrhage, both hormone levels increased, but only OT was further enhanced by L-NAME. Thus cen trally produced NO tonically inhibits OT and VP secretion under basal normovolemic conditions and selectively inhibits OT release during hyp ovolemia. Hemorrhage increased the rates of glucose utilization in the neural lobe, indicative of enhanced efferent neural functional activi ty. L-NAME further enhanced the metabolic activity in the entire hypot halamoneurohypophysial system of hemorrhaged animals. Several other br ain structures involved in the regulation of blood pressure and the st ress response were also metabolically affected by the hemorrhage and L -NAME.