Effect of vasopressin-induced chronic hyponatremia on the regulation of the middle cerebral artery of the rat.

Vasopressin (arginine vasopressin, AVP) plays a crucial role in maintaining body fluid homeostasis. Excessive release of vasopressin can lead to hyponatremia. Changes in cerebral circulation during vasopressin-induced chronic hyponatremia are not elucidated. The present study has been designed to investigate the effect of chronic vasopressin-induced hyponatremia on the regulation of the tone of the middle cerebral artery (MCA) of the rat. Chronic hyponatremia was induced in vivo with the help of vasopressin, released continuously from subcutaneously implanted ALZET mini-osmotic pumps, and a liquid diet. After 3.5 days of chronic hyponatremia, the plasma Na+ concentration decreased to 119 ± 3 mM. MCAs were isolated and placed in a MOPS-buffered saline solution containing 121 mM Na+. Chronic hyponatremia did not affect the response of the MCA to increased intravascular pressure, to the administration of acetylcholine (ACh) and nitric oxide (NO) donor (SNAP, S-nitroso-N-acetyl-DL-penicillamine), and to increased K+ concentration, but impaired the response of the MCA to increased extravascular H+ concentration. Disturbed response of the MCA to acidosis was associated neither with the impairment of KATP channels nor with the activation of vasopressin V1 receptor. Correction of hyponatremia did not restore the response of the MCA to acidosis. These results indicate that cerebral blood vessels do not fully adapt to prolonged vasopressin-induced hyponatremia.