Analgesia induced by cold water stress (CWS) was tested in the model of monolateral inflammation in spontaneously hypertensive (SHR), renal hypertensive (RHR) and normotensive Wistar (NR) and Wistar Kyoto (WKY) rats. Unilateral hind paw inflammation was induced by Freund's complete adjuvant (FCA). Four days after inoculation all tested rats exhibited profound analgesia following CWS in both inflamed and non-inflamed paws which reached a maximum immediately after CWS and returned to control values within 15 min. The activity of naloxone was tested both by systemic and local injection. Baseline pain thresholds of SHR rats were significantly higher than those of NR, WKY and RHR. Hyperalgesia following systemic intraperitoneal administration of naloxone applied ten minutes before CWS was higher in RHR and WKY than in NR and SHR. When administered directly into the inflamed paw, naloxone did not antagonize CWS-induced analgesia in RHR, in contrast to weak antagonism in NR, while more evident in SHR and WKY. Our results probably reflect biological and genetic variability of intrinsic opioid and inflammatory mechanisms in hypertension.