title: Cerebrospinal fluid sodium concentration and osmosensitive sites related to arterial pressure in anaesthetized rats.
abstract: Intracerebroventricular injection of hypertonic saline induces experimental hypertension. To measure [Na] in the vicinity of osmosensitive sites, we continuously measured [Na] in cerebrospinal fluid ([Na]csf) in the lateral ventricle (LV, n = 6), in the third ventricle (V3, n = 6) and in the medial preoptic nucleus (MPO, n = 6) ([Na]MPO) with a Na-sensitive electrode together with mean arterial pressure (MAP) during infusion of hypertonic artificial cerebrospinal fluid (ACSF, [Na] = 1,000 meq/kg H2O) at 5 "mu"l/min for 3 min into the LV in urethane- anaesthetized rats. [Na]csf in the LV began to increase at the beginning of infusion, reaching a peak of 48 +/- 9 meq/kg H2O (mean +/- SE) around the end of infusion, then recovering to the pre-infusion level by 17 min. [Na]csf in V3 changed similarly to that in the LV without any delay, although the peak value was reduced (61% , P < 0.05). In the MPO, in contrast the increase in [Na]MPO was delayed (3 min, P < 0.002) and the peak reduced even further (to 37%, P < 0.01) compared with that in V3. Thereafter, it remained higher than the pre-infusion level until the end of recovery (P < 0.05). MAP began to increase at the onset of infusion (P < 0.05); the maximum increase of 16 +/- 2 mm Hg (n = 18) was reached at the end of infusion, whereafter this level was almost sustained until the end of the 22-min recovery period. To analyse quantitatively the relationship between MAP and [Na]csf, hypertonic ACSF was infused at 2.5 "mu"l/min into the LV. [Na]csf in the LV and MAP increased at half the rates seen with 5 "mu"l/min. These results suggest that the first increase in MAP after hypertonic infusion into the LV is due to the increase in [Na] in the LV and V3, and that the subsequent sustained increase in MAP is related to the delayed increase in [Na] in the periventricular tissues of the V3.
authors.affiliation: Department of Physiology, Kyoto Prefectural University of Medicine, Kawaramachi, Kamigyoku, Kyoto 602, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Hirose
authors.forename: H
authors.initials: H
authors.lastname: Nose
authors.forename: M
authors.initials: M
authors.lastname: Chen
authors.forename: T
authors.initials: T
authors.lastname: Yawata
mesh_terms: D000758:Anesthesia; D000818:Animals; D001665:Binding Sites; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002552:Cerebral Ventricles / Q000187:drug effects / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000134:cerebrospinal fluid / Q000209:etiology; D007276:Injections, Intraventricular; D007427:Intracranial Pressure / Q000187:drug effects / Q000502:physiology; D008297:Male; D008839:Microelectrodes; D051381:Rats; D017208:Rats, Wistar; D012462:Saline Solution, Hypertonic / Q000008:administration & dosage; D012964:Sodium / Q000134:cerebrospinal fluid*; D014882:Water-Electrolyte Balance / Q000502:physiology
chemical_list: D012462:Saline Solution, Hypertonic; D012964:Sodium