title: Effects of L-NAME on cerebral metabolic, vasopressin, oxytocin, and blood pressure responses in hemorrhaged rats.
abstract: NG-nitro-L-arginine methyl ester (L-NAME; 250 micrograms/5 microliters), an inhibitor of NO synthase, or the vehicle artificial cerebrospinal fluid (aCSF; 5 microliters) was administered intracerebroventricularly to conscious rats hemorrhaged (0.7 ml/min) to a 20% volume depletion. Hypotension was maximal 5 min after hemorrhage ended, with compensatory recovery to basal levels 20 min later, regardless of drug treatment. L-NAME, however, elevated (P < 0.05) blood pressure (vs. aCSF controls) 40-45 min after intracerebroventricular administration. In normovolemic rats, L-NAME produced a significant pressor 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 centrally produced NO tonically inhibits OT and VP secretion under basal normovolemic conditions and selectively inhibits OT release during hypovolemia. Hemorrhage increased the rates of glucose utilization in the neural lobe, indicative of enhanced efferent neural functional activity. L-NAME further enhanced the metabolic activity in the entire hypothalamoneurohypophysial system of hemorrhaged animals. Several other brain structures involved in the regulation of blood pressure and the stress response were also metabolically affected by the hemorrhage and L-NAME.
authors.affiliation: Division of Neurosurgery, University of Texas Medical Branch at Galveston 77555-0517, USA.
authors.forename: M
authors.initials: M
authors.lastname: Kadekaro
authors.forename: M L
authors.initials: ML
authors.lastname: Terrell
authors.forename: H
authors.initials: H
authors.lastname: Liu
authors.forename: S
authors.initials: S
authors.lastname: Gestl
authors.forename: V
authors.initials: V
authors.lastname: Bui
authors.forename: J Y
authors.initials: JY
authors.lastname: Summy-Long
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001826:Body Fluids / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D003847:Deoxyglucose / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism; D006470:Hemorrhage / Q000097:blood / Q000503:physiopathology*; D006706:Homeostasis / Q000502:physiology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D009569:Nitric Oxide / Q000502:physiology; D010121:Oxytocin / Q000097:blood*; D010904:Pituitary Gland, Posterior / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014667:Vasopressins / Q000097:blood*
chemical_list: D004791:Enzyme Inhibitors; D014667:Vasopressins; D009569:Nitric Oxide; D010121:Oxytocin; D003847:Deoxyglucose; D005947:Glucose; D019331:NG-Nitroarginine Methyl Ester