Changes in either plasma sodium concentration or arterial pressure can differentially affect hypothalamic neurons. For instance, increases in plasma NaCl concentration decrease noradrenaline release from nerve terminals in the anterior hypothalamic nucleus, while increases in arterial pressure unrelated to an elevation in plasma NaCl enhance noradrenaline release in anterior hypothalamic nucleus. The present study tests the hypothesis that in the rat the organum vasculosum of the lamina terminalis (an osmosensitive area of the brain) detects rises in plasma NaCl concentration and conveys this information to anterior hypothalamic nucleus. The axons projecting from the organum vasculosum of the lamina terminalis to the hypothalamus were unilaterally cut immediately caudal to organum vasculosum of the lamina terminalis, and five days later, 3-methoxy-4-hydroxy phenylglycol (the major metabolite of noradrenaline in brain) was continuously monitored in the ipsilateral or contralateral anterior hypothalamic nucleus in response to an intravenous infusion of hypertonic saline. In spontaneously hypertensive rats, the infusion decreased the 3-methoxy-4-hydroxy phenylglycol concentration by 24+/-2% in the anterior hypothalamic nucleus contralateral to the lesion, and in control spontaneously hypertensive rats. In contrast, in the anterior hypothalamic nucleus ipsilateral to the lesion, hypertonic saline infusion caused a 58+/-3% increase in 3-methoxy-4-hydroxy phenylglycol. These data support the hypothesis that the organum vasculosum of the lamina terminalis is part of the circuit that transmits information concerning plasma NaCl concentration to anterior hypothalamic nucleus.