of Ͻ6°C or Ͼ29°C have been shown to induce large changes in arterial blood pressure and heart rate in homeotherms. The present study was designed to investigate whether small incremental changes in T a, such as those found in typical laboratory settings, would have an impact on blood pressure and other cardiovascular parameters in mice and rats. We predicted that small decreases in T a would impact the cardiovascular parameters of mice more than rats due to the increased thermogenic demands resulting from a greater surface area-to-volume ratio in mice relative to rats. Cardiovascular parameters were measured with radiotelemetry in mice and rats that were housed in temperaturecontrolled environments. The animals were exposed to different T a every 72 h, beginning at 30°C and incrementally decreasing by 4°C at each time interval to 18°C and then incrementally increasing back up to 30°C. As T a decreased, mean blood pressure, heart rate, and pulse pressure increased significantly for both mice (1.6 mmHg/°C, 14.4 beats ⅐ min Ϫ1 ⅐°C Ϫ1 , and 0.8 mmHg/°C, respectively) and rats (1.2 mmHg/°C, 8.1 beats ⅐ min Ϫ1 ⅐°C Ϫ1 , and 0.8 mmHg/°C, respectively). Thus small changes in T a significantly impact the cardiovascular parameters of both rats and mice, with mice demonstrating a greater sensitivity to these Ta changes. blood pressure; heart rate; standard deviation of the interbeat interval; radiotelemetry THE EXTERNAL ENVIRONMENT can have a substantial impact on the cardiovascular system. Exposure of humans (1,7,18,32), rats (2,3,14,20), and mice (22) to cold ambient temperature (T a ) results in elevated blood pressure and heart rate. It appears as if the tachycardia and hypertension are the indirect result of sympathetic nervous system (SNS) activation of thermoregulatory mechanisms because elevated plasma norepinephrine (NE) levels correlate with elevated blood pressure in the cold (7,14,17,32). Furthermore, propranolol, a -adrenergic blocking agent, can blunt or completely reverse the cardiovascular effects of cold exposure (21). Cold-induced activation of the SNS, in turn, appears to elevate blood pressure through activation of the renin-angiotensin system (RAS). Blockade of the RAS systemically (19), centrally (15,16,22), or genetically in an angiotensinogen knockout mouse model (23) blunts or prevents cold-induced hypertension, suggesting that RAS signaling pathways are necessary for T a -induced effects on blood pressure.Elevation of T a beyond typical housing temperatures also impacts the cardiovascular system. Warming rats (31) and mice (30, 31) from 23°C to 28 -31°C, closer to, if not within, their thermoneutral zone (TNZ) results in a drop in heart rate and blood pressure. Metabolic rate in homeotherms is at its minimum in the TNZ, which is approximately 28 -31°C for rodents (4). Animals with smaller body sizes have higher surface area-to-volume ratios and thus typically exhibit warmer TNZs. At temperatures below the TNZ, nonshivering thermogenesis is stimulated by increased sympathetic activity to offset the...