M. Kadekaro et al., EFFECTS OF L-NAME ON CEREBRAL METABOLIC, VASOPRESSIN, OXYTOCIN, AND BLOOD-PRESSURE RESPONSES IN HEMORRHAGED RATS, American journal of physiology. Regulatory, integrative and comparative physiology, 43(4), 1998, pp. 1070-1077
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.