This study sought to determine whether spontaneously hypertensive rats (SHR) on a high-NaCl diet have an enhanced pressor response to acute cold exposure and to define the peripheral mechanisms involved in the enhanced pressor response. SHR and normotensive Wistar-Kyoto (WKY) rats that had been on 1 and 8% NaCl diets for 3 wk were subjected to cold exposure. After a 30-min control period, animals were exposed to cold (6 ± 2°C) for 90 min. Mean arterial pressure (MAP), heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured continuously. In a separate group of SHR on 1 and 8% NaCl diets, an arginine vasopressin (AVP) V1 receptor antagonist (10 μg/kg iv) was given before cold exposure, and MAP was measured throughout cold exposure. Plasma AVP was measured before and during cold exposure in a separate group of SHR. During cold exposure, there was a significant increase (P < 0.05) in MAP (25 mmHg) in SHR on the 8% NaCl diet only. In contrast, HR and LSNA increased similarly during cold exposure in both SHR and WKY on the two diets. AVP was similar in both SHR groups (7.1 pg/ml for 1% vs. 6.1 pg/ml for 8%) before cold exposure, but during cold exposure it increased in the 8% NaCl SHR only, reaching 17.6 pg/ml at 90 min. The AVP V1 antagonist completely abolished the cold stress-induced rise in MAP in SHR. Thus SHR on a high-NaCl diet have an enhanced pressor response to acute cold exposure compared with SHR on a normal NaCl diet. The enhanced response does not appear to be due to an exaggerated increase in sympathetic nerve activity but rather to increased circulating AVP levels.