Suppression of basal NO- and prostacyclin-dependent tone in cerebral microcirculation during chronic hyponatremia in female rats.

BACKGROUND: Our previous studies in the rat model of chronic hyponatremia have demonstrated the decrease of cerebral blood flow along with the attenuation of cerebral metabolic rate for oxygen exclusively in females and when hyponatremia was induced with vasopressin. Present study was designed to verify the hypothesis that the decrease of cerebral blood flow during chronic vasopressin-induced hyponatremia in female rats is due to the attenuation of basal vasodilator tone produced in cerebral microcirculation under physiological conditions by shear-stress-dependent release of nitric oxide and prostacyclin. MATERIAL AND METHODS: The experiments were performed on 47 anesthetized and mechanically ventilated adult, female Wistar rats. Chronic hyponatremia (3.5 days) was induced in these rats by the twice-daily subcutaneous administration of vasopressin (AVP) in conjunction with 140 mmol/L glucose/water solution. Cerebrocortical microflow (LDF) was monitored using laser-Doppler probe. LDF responses to the administration 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% CO2 were tested in normonatremic and hyponatremic rats. RESULTS: The response of LDF to L-NAME, INDO and ACh were abolished in rats with hyponatremia. In contrast, CO2 reactivity was well preserved. CONCLUSIONS: Our results demonstrate that attenuation of cerebral blood flow during chronic AVP-induced hyponatremia in female rats is, at least in part, due to the withdrawal of basal vasodilator tone produced in cerebral circulation under physiological conditions by nitric oxide and prostacyclin.