To explore the potential role of norepinephrine (NE) and nitric oxide (NO) in activities of rat hypothalamus arginine vasopressin (AVP) neurons in response to immune challenge, we observed the effect of prazosin, an antagonist of alpha1-adrenergic receptor, and the specific nitric oxide synthase (NOS) inhibitor N(w)nitro-L-arginine-methylester (L-NAME) on the Fos expression in AVP neurons induced by systemic lipopolysaccharide (LPS) using double immunohistochemistry. Intravenous (i.v.) injection of LPS induced Fos expression in AVP neurons mainly in the hypothalamus paraventricular nucleus (PVN) and in the supraoptic nucleus (SON). The percentage of Fos-positive AVP neurons was dose-dependent. Pretreatment with prazosin (5 mg/kg) effectively suppressed the Fos expression induced by LPS (5 microg/kg), whereas L-NAME (30 mg/kg) did not influence the Fos expression in the AVP neurons induced by LPS (0.25, 0.5, 1, 5 microg/kg). Our results suggest that the activation of central AVP neurons caused by systemic LPS may be mediated by NE through alpha1-adrenergic receptors, but could not be changed by NO.