BACKGROUND: Our previous studies in the rat model of chronic hyponatremiahave demonstrated the decrease of cerebral blood flow along with the attenuation of cerebral metabolicrate for oxygen exclusively in females and when hyponatremia was induced with vasopressin. Present studywas designed to verify the hypothesis that the decrease of cerebral blood flow during chronic vasopressin-inducedhyponatremia in female rats is due to the attenuation of basal vasodilator tone produced in cerebralmicrocirculation under physiological conditions by shear-stress-dependent release of nitric oxide andprostacyclin.

MATERIAL AND METHODS: The experiments were performed on 47 anesthetized and mechanicallyventilated adult, female Wistar rats. Chronic hyponatremia (3.5 days) was induced in these rats by thetwice-daily subcutaneous administration of vasopressin (AVP) in conjunction with 140 mmol/L glucose/watersolution. Cerebrocortical microflow (LDF) was monitored using laser-Doppler probe. LDF responses to theadministration of either NG-nitro-L-arginine methyl esther (L-NAME, 30 mg/kg i.v.), indomethacin (INDO,6 mg/kg i.v.), acetylcholine (ACh, 10 Kl/20 Kl/min ica) or 5% CO[sub]2[/sub] were tested in normonatremic and hyponatremicrats.
RESULTS: The response of LDF to L-NAME, INDO and ACh were abolished in rats with hyponatremia. Incontrast, CO[sub]2[/sub] reactivity was well preserved.

CONCLUSIONS: Our results demonstrate that attenuation ofcerebral blood flow during chronic AVP-induced hyponatremia in female rats is, at least in part, dueto the withdrawal of basal vasodilator tone produced in cerebral circulation under physiological conditionsby nitric oxide and prostacyclin.

Keywords: chronic hyponatremia, cerebral microcirculation, L-NAME, Indomethacin, female gender, vasopressin